Žakula, Zorica

Link to this page

Authority KeyName Variants
81d270e9-79d9-4d62-8de7-fa8a561e3dda
  • Žakula, Zorica (31)

Author's Bibliography

Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats

Romić, Snježana Đ.; Tepavčević, Snežana; Žakula, Zorica; Milosavljević, Tijana; Kostić, Milan; Petković, Marijana; Korićanac, Goran

(2014)

TY  - JOUR
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Kostić, Milan
AU  - Petković, Marijana
AU  - Korićanac, Goran
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/6053
AB  - To give new insight to alterations of cardiac lipid metabolism accompanied by a fructose-rich diet (FRD), rats of both sexes were exposed to 10 % fructose in drinking water during 9 weeks. The protein level and subcellular localization of the main regulators of cardiac lipid metabolism, such as lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha), carnitine palmitoyltransferase I (CPTI), and CD36 were studied. Caloric intake in fructose-fed rats (FFR) of both sexes was increased. Circulating triacylglyceroles (TAG) and non-esterified fatty acids were increased in male FFR, while females increased visceral adiposity and blood TAG. Total expression of lipin 1 in cardiac cell lysate and its cytosolic and microsomal level were increased in the hearts of male FFR. PPAR alpha and PGC-1 alpha content were decreased in the nuclear extract. In addition, cardiac deposition of TAG in male FFR was elevated, as well as inhibitory phosphorylation of insulin receptor substrate 1 (IRS-1). In contrast, in female FFR, lipin 1 level was increased in nuclear extract only, while overall CPTI expression and phosphorylation of IRS-1 at serine 307 were decreased. The results of our study suggest that fructose diet causes gender-dependent alterations in cardiac lipid metabolism. Potentially detrimental effects of FRD seem to be limited to male rats. Most of the observed changes might be a consequence of elevated expression and altered localization of lipin 1. Increased inhibitory phosphorylation of IRS-1 is possible link between cardiac lipid metabolism and insulin resistance in FFR.
T2  - Lipids
T1  - Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats
VL  - 49
IS  - 7
SP  - 655
EP  - 663
DO  - 10.1007/s11745-014-3909-4
ER  - 
@article{
author = "Romić, Snježana Đ. and Tepavčević, Snežana and Žakula, Zorica and Milosavljević, Tijana and Kostić, Milan and Petković, Marijana and Korićanac, Goran",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/6053",
abstract = "To give new insight to alterations of cardiac lipid metabolism accompanied by a fructose-rich diet (FRD), rats of both sexes were exposed to 10 % fructose in drinking water during 9 weeks. The protein level and subcellular localization of the main regulators of cardiac lipid metabolism, such as lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha), carnitine palmitoyltransferase I (CPTI), and CD36 were studied. Caloric intake in fructose-fed rats (FFR) of both sexes was increased. Circulating triacylglyceroles (TAG) and non-esterified fatty acids were increased in male FFR, while females increased visceral adiposity and blood TAG. Total expression of lipin 1 in cardiac cell lysate and its cytosolic and microsomal level were increased in the hearts of male FFR. PPAR alpha and PGC-1 alpha content were decreased in the nuclear extract. In addition, cardiac deposition of TAG in male FFR was elevated, as well as inhibitory phosphorylation of insulin receptor substrate 1 (IRS-1). In contrast, in female FFR, lipin 1 level was increased in nuclear extract only, while overall CPTI expression and phosphorylation of IRS-1 at serine 307 were decreased. The results of our study suggest that fructose diet causes gender-dependent alterations in cardiac lipid metabolism. Potentially detrimental effects of FRD seem to be limited to male rats. Most of the observed changes might be a consequence of elevated expression and altered localization of lipin 1. Increased inhibitory phosphorylation of IRS-1 is possible link between cardiac lipid metabolism and insulin resistance in FFR.",
journal = "Lipids",
title = "Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats",
volume = "49",
number = "7",
pages = "655-663",
doi = "10.1007/s11745-014-3909-4"
}
Romić, S. Đ., Tepavčević, S., Žakula, Z., Milosavljević, T., Kostić, M., Petković, M.,& Korićanac, G. (2014). Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats.
Lipids, 49(7), 655-663.
https://doi.org/10.1007/s11745-014-3909-4
Romić SĐ, Tepavčević S, Žakula Z, Milosavljević T, Kostić M, Petković M, Korićanac G. Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats. Lipids. 2014;49(7):655-663
Romić Snježana Đ., Tepavčević Snežana, Žakula Zorica, Milosavljević Tijana, Kostić Milan, Petković Marijana, Korićanac Goran, "Gender Differences in the Expression and Cellular Localization of Lipin 1 in the Hearts of Fructose-Fed Rats" Lipids, 49, no. 7 (2014):655-663,
https://doi.org/10.1007/s11745-014-3909-4 .
5
5
5

Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol

Korićanac, Goran; Tepavčević, Snežana; Romić, Snježana Đ.; Milosavljević, Tijana; Stojiljković, Mojca D.; Žakula, Zorica

(2014)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Romić, Snježana Đ.
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5879
T2  - Hormone and Metabolic Research
T1  - Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol
VL  - 46
IS  - 2
SP  - 109
EP  - 115
ER  - 
@article{
author = "Korićanac, Goran and Tepavčević, Snežana and Romić, Snježana Đ. and Milosavljević, Tijana and Stojiljković, Mojca D. and Žakula, Zorica",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5879",
journal = "Hormone and Metabolic Research",
title = "Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol",
volume = "46",
number = "2",
pages = "109-115"
}
Korićanac, G., Tepavčević, S., Romić, S. Đ., Milosavljević, T., Stojiljković, M. D.,& Žakula, Z. (2014). Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol.
Hormone and Metabolic Research, 46(2), 109-115.
Korićanac G, Tepavčević S, Romić SĐ, Milosavljević T, Stojiljković MD, Žakula Z. Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol. Hormone and Metabolic Research. 2014;46(2):109-115
Korićanac Goran, Tepavčević Snežana, Romić Snježana Đ., Milosavljević Tijana, Stojiljković Mojca D., Žakula Zorica, "Expression and Cellular Distribution of Glucose Transporters and Alpha Subunits of Na+/K+-ATPase in the Heart of Fructose-fed Female Rats: The Role of Estradiol" Hormone and Metabolic Research, 46, no. 2 (2014):109-115
7

Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome

Tepavčević, Snežana; Milutinovic, Danijela Vojnovic; Macut, Djuro; Žakula, Zorica; Nikolic, Marina; Bozic-Antic, Ivana; Romić, Snježana Đ.; Bjekic-Macut, Jelica; Matić, Gordana; Korićanac, Goran

(2014)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, Danijela Vojnovic
AU  - Macut, Djuro
AU  - Žakula, Zorica
AU  - Nikolic, Marina
AU  - Bozic-Antic, Ivana
AU  - Romić, Snježana Đ.
AU  - Bjekic-Macut, Jelica
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5970
AB  - It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphoiylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action. (c) 2014 Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome
VL  - 141
SP  - 71
EP  - 76
DO  - 10.1016/j.jsbmb.2014.01.006
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, Danijela Vojnovic and Macut, Djuro and Žakula, Zorica and Nikolic, Marina and Bozic-Antic, Ivana and Romić, Snježana Đ. and Bjekic-Macut, Jelica and Matić, Gordana and Korićanac, Goran",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5970",
abstract = "It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphoiylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action. (c) 2014 Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome",
volume = "141",
pages = "71-76",
doi = "10.1016/j.jsbmb.2014.01.006"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Žakula, Z., Nikolic, M., Bozic-Antic, I., Romić, S. Đ., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2014). Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome.
Journal of Steroid Biochemistry and Molecular Biology, 141, 71-76.
https://doi.org/10.1016/j.jsbmb.2014.01.006
Tepavčević S, Milutinovic DV, Macut D, Žakula Z, Nikolic M, Bozic-Antic I, Romić SĐ, Bjekic-Macut J, Matić G, Korićanac G. Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome. Journal of Steroid Biochemistry and Molecular Biology. 2014;141:71-76
Tepavčević Snežana, Milutinovic Danijela Vojnovic, Macut Djuro, Žakula Zorica, Nikolic Marina, Bozic-Antic Ivana, Romić Snježana Đ., Bjekic-Macut Jelica, Matić Gordana, Korićanac Goran, "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome" Journal of Steroid Biochemistry and Molecular Biology, 141 (2014):71-76,
https://doi.org/10.1016/j.jsbmb.2014.01.006 .
12
11
12

Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats

Korićanac, Goran; Đorđević, Ana D.; Žakula, Zorica; Vojnovic-Milutinovic, Danijela; Tepavčević, Snežana; Velikovic, Natasa; Milosavljević, Tijana; Stojiljković, Mojca D.; Romić, Snježana Đ.; Matić, Gordana

(2013)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Đorđević, Ana D.
AU  - Žakula, Zorica
AU  - Vojnovic-Milutinovic, Danijela
AU  - Tepavčević, Snežana
AU  - Velikovic, Natasa
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Romić, Snježana Đ.
AU  - Matić, Gordana
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5507
AB  - We analyzed the effects of a fructose-rich diet (FRD) to test the assumption that the expression of metabolic syndrome phenotype is different in male and female rats. Two-way ANOVA revealed a significant effect of FRD on feeding behavior and carbohydrate/lipid metabolism. The increased caloric intake in FRD rats of both sexes was followed by a cluster of gender-specific changes typical for the metabolic syndrome. Female rats were characterized by decreased glycemia, increased triglycerides, enlarged visceral adipose tissue and increased absolute mass of liver, without changes in systolic blood pressure and insulin sensitivity. In contrast, male rats developed less disturbances in physical and biochemical characteristics, but blood pressure and insulin sensitivity were impaired by FRD. The results emphasize the detrimental effects of fructose consumption on cardiovascular risk and insulin action in males, whereas females are affected by other metabolic disturbances. These results support the idea of gender-dependent differences in the expression of the metabolic syndrome phenotype.
T2  - Archives of biological sciences
T1  - Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats
VL  - 65
IS  - 2
SP  - 455
EP  - 464
DO  - 10.2298/ABS1302455K
ER  - 
@article{
author = "Korićanac, Goran and Đorđević, Ana D. and Žakula, Zorica and Vojnovic-Milutinovic, Danijela and Tepavčević, Snežana and Velikovic, Natasa and Milosavljević, Tijana and Stojiljković, Mojca D. and Romić, Snježana Đ. and Matić, Gordana",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5507",
abstract = "We analyzed the effects of a fructose-rich diet (FRD) to test the assumption that the expression of metabolic syndrome phenotype is different in male and female rats. Two-way ANOVA revealed a significant effect of FRD on feeding behavior and carbohydrate/lipid metabolism. The increased caloric intake in FRD rats of both sexes was followed by a cluster of gender-specific changes typical for the metabolic syndrome. Female rats were characterized by decreased glycemia, increased triglycerides, enlarged visceral adipose tissue and increased absolute mass of liver, without changes in systolic blood pressure and insulin sensitivity. In contrast, male rats developed less disturbances in physical and biochemical characteristics, but blood pressure and insulin sensitivity were impaired by FRD. The results emphasize the detrimental effects of fructose consumption on cardiovascular risk and insulin action in males, whereas females are affected by other metabolic disturbances. These results support the idea of gender-dependent differences in the expression of the metabolic syndrome phenotype.",
journal = "Archives of biological sciences",
title = "Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats",
volume = "65",
number = "2",
pages = "455-464",
doi = "10.2298/ABS1302455K"
}
Korićanac, G., Đorđević, A. D., Žakula, Z., Vojnovic-Milutinovic, D., Tepavčević, S., Velikovic, N., Milosavljević, T., Stojiljković, M. D., Romić, S. Đ.,& Matić, G. (2013). Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats.
Archives of biological sciences, 65(2), 455-464.
https://doi.org/10.2298/ABS1302455K
Korićanac G, Đorđević AD, Žakula Z, Vojnovic-Milutinovic D, Tepavčević S, Velikovic N, Milosavljević T, Stojiljković MD, Romić SĐ, Matić G. Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats. Archives of biological sciences. 2013;65(2):455-464
Korićanac Goran, Đorđević Ana D., Žakula Zorica, Vojnovic-Milutinovic Danijela, Tepavčević Snežana, Velikovic Natasa, Milosavljević Tijana, Stojiljković Mojca D., Romić Snježana Đ., Matić Gordana, "Gender Modulates Development of the Metabolic Syndrome Phenotype in Fructose-Fed Rats" Archives of biological sciences, 65, no. 2 (2013):455-464,
https://doi.org/10.2298/ABS1302455K .
12
12
12

Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?

Romić, Snježana Đ.; Tepavčević, Snežana; Žakula, Zorica; Milosavljević, Tijana; Stojiljković, Mojca D.; Živković, Maja; Popović, Milan; Stanković, Aleksandra; Korićanac, Goran

(2013)

TY  - JOUR
AU  - Romić, Snježana Đ.
AU  - Tepavčević, Snežana
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Živković, Maja
AU  - Popović, Milan
AU  - Stanković, Aleksandra
AU  - Korićanac, Goran
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5513
AB  - Fructose-rich diets (FRD) cause cardiac insulin resistance manifested by impairment of Akt/endothelial NO synthase (eNOS) signalling. In contrast, oestradiol (E2) activates this signalling pathway in the heart. To study the ability of E2 to revert the detrimental effect of fructose on cardiac Akt/eNOS, female rats were subjected to a FRD and ovariectomy followed with or without E2 replacement. We also analysed the effects of the FRD and E2 on cardiac extracellular signal-regulated kinase (Erk 1/2) signalling related to their role in cardiac hypertrophy development. Expression of Akt, eNOS and Erk 1/2, as well as regulatory phosphorylations of these molecules were determined. The protein expression of cardiac Akt and eNOS was not affected by the diet or E2 treatment. However, the FRD was accompanied by a decrease in Akt phosphorylation at Ser(473) and Thr(308), and eNOS at Ser(1177), while the phosphorylation of eNOS at Thr(495) was increased. E2 replacement in ovariectomised fructose-fed rats caused a reversion of the diet effect on Akt and eNOS serine phosphorylation, but mostly had no effect on threonine phosphorylation of the molecules. The FRD and E2 treatment did not influence Erk 1/2 expression and phosphorylation and heart mass as well. The data show that E2 selectively suppress the negative effects of a FRD on Akt/eNOS signalling and probably point to the different effects of E2 on kinase/phosphatase pathways responsible for phosphorylation/dephosphorylation of Akt and eNOS. Furthermore, the results suggest that the heart of females in the reproductive period is partially protected against the damaging effects of increased fructose intake.
T2  - British Journal of Nutrition
T1  - Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?
VL  - 109
IS  - 11
SP  - 1940
EP  - 1948
DO  - 10.1017/S0007114512004114
ER  - 
@article{
author = "Romić, Snježana Đ. and Tepavčević, Snežana and Žakula, Zorica and Milosavljević, Tijana and Stojiljković, Mojca D. and Živković, Maja and Popović, Milan and Stanković, Aleksandra and Korićanac, Goran",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5513",
abstract = "Fructose-rich diets (FRD) cause cardiac insulin resistance manifested by impairment of Akt/endothelial NO synthase (eNOS) signalling. In contrast, oestradiol (E2) activates this signalling pathway in the heart. To study the ability of E2 to revert the detrimental effect of fructose on cardiac Akt/eNOS, female rats were subjected to a FRD and ovariectomy followed with or without E2 replacement. We also analysed the effects of the FRD and E2 on cardiac extracellular signal-regulated kinase (Erk 1/2) signalling related to their role in cardiac hypertrophy development. Expression of Akt, eNOS and Erk 1/2, as well as regulatory phosphorylations of these molecules were determined. The protein expression of cardiac Akt and eNOS was not affected by the diet or E2 treatment. However, the FRD was accompanied by a decrease in Akt phosphorylation at Ser(473) and Thr(308), and eNOS at Ser(1177), while the phosphorylation of eNOS at Thr(495) was increased. E2 replacement in ovariectomised fructose-fed rats caused a reversion of the diet effect on Akt and eNOS serine phosphorylation, but mostly had no effect on threonine phosphorylation of the molecules. The FRD and E2 treatment did not influence Erk 1/2 expression and phosphorylation and heart mass as well. The data show that E2 selectively suppress the negative effects of a FRD on Akt/eNOS signalling and probably point to the different effects of E2 on kinase/phosphatase pathways responsible for phosphorylation/dephosphorylation of Akt and eNOS. Furthermore, the results suggest that the heart of females in the reproductive period is partially protected against the damaging effects of increased fructose intake.",
journal = "British Journal of Nutrition",
title = "Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?",
volume = "109",
number = "11",
pages = "1940-1948",
doi = "10.1017/S0007114512004114"
}
Romić, S. Đ., Tepavčević, S., Žakula, Z., Milosavljević, T., Stojiljković, M. D., Živković, M., Popović, M., Stanković, A.,& Korićanac, G. (2013). Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?.
British Journal of Nutrition, 109(11), 1940-1948.
https://doi.org/10.1017/S0007114512004114
Romić SĐ, Tepavčević S, Žakula Z, Milosavljević T, Stojiljković MD, Živković M, Popović M, Stanković A, Korićanac G. Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?. British Journal of Nutrition. 2013;109(11):1940-1948
Romić Snježana Đ., Tepavčević Snežana, Žakula Zorica, Milosavljević Tijana, Stojiljković Mojca D., Živković Maja, Popović Milan, Stanković Aleksandra, Korićanac Goran, "Does oestradiol attenuate the damaging effects of a fructose-rich diet on cardiac Akt/endothelial nitric oxide synthase signalling?" British Journal of Nutrition, 109, no. 11 (2013):1940-1948,
https://doi.org/10.1017/S0007114512004114 .
1
10
9
9

Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity

Stojiljković, Mojca D.; Žakula, Zorica; Korićanac, Goran; Milosavljević, Tijana; Tepavčević, Snežana; Sudar, Emina; Isenović, Esma R.

(2012)

TY  - JOUR
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Milosavljević, Tijana
AU  - Tepavčević, Snežana
AU  - Sudar, Emina
AU  - Isenović, Esma R.
PY  - 2012
UR  - http://openurl.ingenta.com/content/xref?genre=article&issn=1936-6612&volume=5&issue=2&spage=566
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7801
AB  - The aim of our study was to characterize the acute effects of streptozotocin-induced diabetes on the regulation of cardiac endothelial and inducibile nitric oxide synthase and related signaling pathways. Over the past decade, it has become increasing apparent that competition between the nitric oxide synthase and arginase pathways for L-arginin limits nitric oxid production. Imbalance between these pathways may contribute to heart disfunction especially in diabetes. To evaluate the role of insulin in regulation of endothelial and inducible nitric oxide synthase through phosphatidylinositol 3-kinase/protein kinase B and extracellular signaling-regulated kinase 1 and 2 signaling pathways, male Wistar rats were injected with streptozotocin (65 mg/kg i.p.). Diabetic animals were either maintained untreated for 2 weeks or treated with insulin (3 IU/animal s.c.) for seven days. The arginase activity in diabetic rat heart was augmented, followed by reduction of L-arginine. Insulin treatment significantly decreased arginase activity in heart but it still remained high compare to control rats. Diabetes and insulin treatment did not change endothelial nitric oxide synthase protein and mRNA expression in the heart. In contrast, phosphorylation of endothelial nitric oxide synthase was decreased in diabetic rats and insulin restored it to the control level. Insulin treatment caused increase in inducibile nitric oxide synthase mRNA content. Protein and mRNA expression of cardiac protein kinase B were not altered in diabetic and insulin treated rats, but protein kinase B phosphorylation was lower in diabetes and restored after insulin administration. In addition, insulin deficiency significantly decreases extracellular signaling-regulated kinase 1 and 2 phosphorylation in the heart and insulin treatment partially ameliorates this decline. These data suggest that in the early stage of diabetes arginase is markedly induced in heart and increased arginase activity preceded alterations of inducibile nitric oxide synthase expression/activity. © 2012 American Scientific Publishers All rights reserved.
T2  - Advanced Science Letters
T1  - Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity
VL  - 5
IS  - 2
SP  - 566
EP  - 574
DO  - 10.1166/asl.2012.3254
ER  - 
@article{
author = "Stojiljković, Mojca D. and Žakula, Zorica and Korićanac, Goran and Milosavljević, Tijana and Tepavčević, Snežana and Sudar, Emina and Isenović, Esma R.",
year = "2012",
url = "http://openurl.ingenta.com/content/xref?genre=article&issn=1936-6612&volume=5&issue=2&spage=566, http://vinar.vin.bg.ac.rs/handle/123456789/7801",
abstract = "The aim of our study was to characterize the acute effects of streptozotocin-induced diabetes on the regulation of cardiac endothelial and inducibile nitric oxide synthase and related signaling pathways. Over the past decade, it has become increasing apparent that competition between the nitric oxide synthase and arginase pathways for L-arginin limits nitric oxid production. Imbalance between these pathways may contribute to heart disfunction especially in diabetes. To evaluate the role of insulin in regulation of endothelial and inducible nitric oxide synthase through phosphatidylinositol 3-kinase/protein kinase B and extracellular signaling-regulated kinase 1 and 2 signaling pathways, male Wistar rats were injected with streptozotocin (65 mg/kg i.p.). Diabetic animals were either maintained untreated for 2 weeks or treated with insulin (3 IU/animal s.c.) for seven days. The arginase activity in diabetic rat heart was augmented, followed by reduction of L-arginine. Insulin treatment significantly decreased arginase activity in heart but it still remained high compare to control rats. Diabetes and insulin treatment did not change endothelial nitric oxide synthase protein and mRNA expression in the heart. In contrast, phosphorylation of endothelial nitric oxide synthase was decreased in diabetic rats and insulin restored it to the control level. Insulin treatment caused increase in inducibile nitric oxide synthase mRNA content. Protein and mRNA expression of cardiac protein kinase B were not altered in diabetic and insulin treated rats, but protein kinase B phosphorylation was lower in diabetes and restored after insulin administration. In addition, insulin deficiency significantly decreases extracellular signaling-regulated kinase 1 and 2 phosphorylation in the heart and insulin treatment partially ameliorates this decline. These data suggest that in the early stage of diabetes arginase is markedly induced in heart and increased arginase activity preceded alterations of inducibile nitric oxide synthase expression/activity. © 2012 American Scientific Publishers All rights reserved.",
journal = "Advanced Science Letters",
title = "Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity",
volume = "5",
number = "2",
pages = "566-574",
doi = "10.1166/asl.2012.3254"
}
Stojiljković, M. D., Žakula, Z., Korićanac, G., Milosavljević, T., Tepavčević, S., Sudar, E.,& Isenović, E. R. (2012). Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity.
Advanced Science Letters, 5(2), 566-574.
https://doi.org/10.1166/asl.2012.3254
Stojiljković MD, Žakula Z, Korićanac G, Milosavljević T, Tepavčević S, Sudar E, Isenović ER. Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity. Advanced Science Letters. 2012;5(2):566-574
Stojiljković Mojca D., Žakula Zorica, Korićanac Goran, Milosavljević Tijana, Tepavčević Snežana, Sudar Emina, Isenović Esma R., "Regulation of Cardiac Nitric Oxide Synthase in Acute Type I Diabetes: Modulation of L-Arginine Availability and Arginase Activity" Advanced Science Letters, 5, no. 2 (2012):566-574,
https://doi.org/10.1166/asl.2012.3254 .
1

Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation

Korićanac, Goran; Tepavčević, Snežana; Romić, Snježana Đ.; Živković, Maja; Stojiljković, Mojca D.; Milosavljević, Tijana; Stanković, Aleksandra; Petković, Marijana; Kamceva, Tina; Žakula, Zorica

(2012)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Romić, Snježana Đ.
AU  - Živković, Maja
AU  - Stojiljković, Mojca D.
AU  - Milosavljević, Tijana
AU  - Stanković, Aleksandra
AU  - Petković, Marijana
AU  - Kamceva, Tina
AU  - Žakula, Zorica
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5104
AB  - Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes. (C) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation
VL  - 694
IS  - 1-3
SP  - 127
EP  - 134
DO  - 10.1016/j.ejphar.2012.08.007
ER  - 
@article{
author = "Korićanac, Goran and Tepavčević, Snežana and Romić, Snježana Đ. and Živković, Maja and Stojiljković, Mojca D. and Milosavljević, Tijana and Stanković, Aleksandra and Petković, Marijana and Kamceva, Tina and Žakula, Zorica",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5104",
abstract = "Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes. (C) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation",
volume = "694",
number = "1-3",
pages = "127-134",
doi = "10.1016/j.ejphar.2012.08.007"
}
Korićanac, G., Tepavčević, S., Romić, S. Đ., Živković, M., Stojiljković, M. D., Milosavljević, T., Stanković, A., Petković, M., Kamceva, T.,& Žakula, Z. (2012). Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation.
European Journal of Pharmacology, 694(1-3), 127-134.
https://doi.org/10.1016/j.ejphar.2012.08.007
Korićanac G, Tepavčević S, Romić SĐ, Živković M, Stojiljković MD, Milosavljević T, Stanković A, Petković M, Kamceva T, Žakula Z. Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation. European Journal of Pharmacology. 2012;694(1-3):127-134
Korićanac Goran, Tepavčević Snežana, Romić Snježana Đ., Živković Maja, Stojiljković Mojca D., Milosavljević Tijana, Stanković Aleksandra, Petković Marijana, Kamceva Tina, Žakula Zorica, "Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation" European Journal of Pharmacology, 694, no. 1-3 (2012):127-134,
https://doi.org/10.1016/j.ejphar.2012.08.007 .
14
15
15

Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats

Sudar, Emina; Dobutovic, Branislava; Soskić, Sanja S.; Mandušić, Vesna; Žakula, Zorica; Misirkić, Maja; Vucicevic, Ljubica; Janjetović, Kristina D.; Trajković, Vladimir S.; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2011)

TY  - JOUR
AU  - Sudar, Emina
AU  - Dobutovic, Branislava
AU  - Soskić, Sanja S.
AU  - Mandušić, Vesna
AU  - Žakula, Zorica
AU  - Misirkić, Maja
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Trajković, Vladimir S.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4317
AB  - The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.
T2  - Journal of Physiology and Biochemistry
T1  - Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats
VL  - 67
IS  - 2
SP  - 195
EP  - 204
DO  - 10.1007/s13105-010-0063-1
ER  - 
@article{
author = "Sudar, Emina and Dobutovic, Branislava and Soskić, Sanja S. and Mandušić, Vesna and Žakula, Zorica and Misirkić, Maja and Vucicevic, Ljubica and Janjetović, Kristina D. and Trajković, Vladimir S. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4317",
abstract = "The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.",
journal = "Journal of Physiology and Biochemistry",
title = "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats",
volume = "67",
number = "2",
pages = "195-204",
doi = "10.1007/s13105-010-0063-1"
}
Sudar, E., Dobutovic, B., Soskić, S. S., Mandušić, V., Žakula, Z., Misirkić, M., Vucicevic, L., Janjetović, K. D., Trajković, V. S., Mikhailidis, D. P.,& Isenović, E. R. (2011). Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats.
Journal of Physiology and Biochemistry, 67(2), 195-204.
https://doi.org/10.1007/s13105-010-0063-1
Sudar E, Dobutovic B, Soskić SS, Mandušić V, Žakula Z, Misirkić M, Vucicevic L, Janjetović KD, Trajković VS, Mikhailidis DP, Isenović ER. Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. Journal of Physiology and Biochemistry. 2011;67(2):195-204
Sudar Emina, Dobutovic Branislava, Soskić Sanja S., Mandušić Vesna, Žakula Zorica, Misirkić Maja, Vucicevic Ljubica, Janjetović Kristina D., Trajković Vladimir S., Mikhailidis Dimitri P., Isenović Esma R., "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats" Journal of Physiology and Biochemistry, 67, no. 2 (2011):195-204,
https://doi.org/10.1007/s13105-010-0063-1 .
21
19
23

Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase

Korićanac, Goran; Tepavčević, Snežana; Žakula, Zorica; Milosavljević, Tijana; Stojiljković, Mojca D.; Isenović, Esma R.

(2011)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4254
AB  - Insulin and estradiol share some of signaling pathways and regulate same target molecules exerting mostly beneficial cardiac effects. in order to study their cardiac interaction, ovariectomized female rats were treated with hormones, separately or simultaneously (20,30 or 40 min before analysis), and the phosphorylations of protein kinase B (Akt), extracellular signal-regulated kinases 1 and 2 (ERK 1/2), endothelial nitric oxide synthase (eNOS) were analyzed, as well as the plasma membrane content of alpha 2 subunit of Na+/K+-ATPase. Insulin, particularly, and estradiol stimulate Ser(473) Akt phosphorylation. The combined treatment was stimulatory, but less than insulin alone was. The general increase of Thr(308) Akt phosphorylation by insulin was stronger than at Ser(473) and reduced in the presence of estradiol, which also stimulated this phosphorylation given alone. The estradiol induction of ERK 1/2 phosphorylation was inverted to the decrease by the combined treatment, while insulin had no effect. Only insulin increased the plasma membrane content of alpha 2. Estradiol did increase the phosphorylation of eNOS, whereas the insulin effect was controversial. The effect of the combined treatment on target molecules was generally opposite to single hormone treatment. In summary, both hormones exerted an effect on Akt phosphorylation, but only estradiol stimulated ERK 1/2 phosphorylation. The alpha 2 plasma membrane content was increased only by insulin, while estradiol increased eNOS phosphorylation more consistently. Finally, if these hormones were administered together, it seems that they disturb each other in having a full effect on cardiac Akt, ERK 1/2, and downstream effectors, eNOS and Na+/K+-ATPase. (c) 2011 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase
VL  - 655
IS  - 1-3
SP  - 23
EP  - 30
DO  - 10.1016/j.ejphar.2011.01.016
ER  - 
@article{
author = "Korićanac, Goran and Tepavčević, Snežana and Žakula, Zorica and Milosavljević, Tijana and Stojiljković, Mojca D. and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4254",
abstract = "Insulin and estradiol share some of signaling pathways and regulate same target molecules exerting mostly beneficial cardiac effects. in order to study their cardiac interaction, ovariectomized female rats were treated with hormones, separately or simultaneously (20,30 or 40 min before analysis), and the phosphorylations of protein kinase B (Akt), extracellular signal-regulated kinases 1 and 2 (ERK 1/2), endothelial nitric oxide synthase (eNOS) were analyzed, as well as the plasma membrane content of alpha 2 subunit of Na+/K+-ATPase. Insulin, particularly, and estradiol stimulate Ser(473) Akt phosphorylation. The combined treatment was stimulatory, but less than insulin alone was. The general increase of Thr(308) Akt phosphorylation by insulin was stronger than at Ser(473) and reduced in the presence of estradiol, which also stimulated this phosphorylation given alone. The estradiol induction of ERK 1/2 phosphorylation was inverted to the decrease by the combined treatment, while insulin had no effect. Only insulin increased the plasma membrane content of alpha 2. Estradiol did increase the phosphorylation of eNOS, whereas the insulin effect was controversial. The effect of the combined treatment on target molecules was generally opposite to single hormone treatment. In summary, both hormones exerted an effect on Akt phosphorylation, but only estradiol stimulated ERK 1/2 phosphorylation. The alpha 2 plasma membrane content was increased only by insulin, while estradiol increased eNOS phosphorylation more consistently. Finally, if these hormones were administered together, it seems that they disturb each other in having a full effect on cardiac Akt, ERK 1/2, and downstream effectors, eNOS and Na+/K+-ATPase. (c) 2011 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase",
volume = "655",
number = "1-3",
pages = "23-30",
doi = "10.1016/j.ejphar.2011.01.016"
}
Korićanac, G., Tepavčević, S., Žakula, Z., Milosavljević, T., Stojiljković, M. D.,& Isenović, E. R. (2011). Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase.
European Journal of Pharmacology, 655(1-3), 23-30.
https://doi.org/10.1016/j.ejphar.2011.01.016
Korićanac G, Tepavčević S, Žakula Z, Milosavljević T, Stojiljković MD, Isenović ER. Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase. European Journal of Pharmacology. 2011;655(1-3):23-30
Korićanac Goran, Tepavčević Snežana, Žakula Zorica, Milosavljević Tijana, Stojiljković Mojca D., Isenović Esma R., "Interference between insulin and estradiol signaling pathways in the regulation of cardiac eNOS and Na+/K+-ATPase" European Journal of Pharmacology, 655, no. 1-3 (2011):23-30,
https://doi.org/10.1016/j.ejphar.2011.01.016 .
15
15
18

Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters

Tepavčević, Snežana; Korićanac, Goran; Žakula, Zorica; Milosavljević, Tijana; Stojiljković, Mojca D.; Isenović, Esma R.

(2011)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Korićanac, Goran
AU  - Žakula, Zorica
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4418
AB  - The estrogen binding to specific extranuclear receptors (ER) activates several intracellular pathways that are activated by insulin as well. Moreover, insulin and estradiol (E2) influence cardiac energy substrates, blood glucose and free fatty acids (FFAs), and both hormones exert cardio-beneficial effects. In view of these facts, we suggest that cross-talk between their signaling pathways might have an important role in regulation of cardiac energy substrate transport. Ovariectomized rats were treated with insulin, estradiol (E2), or their combination 20, 30, or 40 min before analysis of blood glucose and FFA level, as well as cardiac plasma membranes (PM) and low density microsomes (LDM) content of glucose (GLUT4 and GLUT1) and FFA (CD36) transporters. Insulin, given alone, or in combination with E2, decreased plasma glucose level at all time points, but did not influence FFA level, while E2 treatment itself did not change glucose and FFA concentration. Insulin increased PM GLUT4 and GLUT1 content 30 and 40 min after treatment and the increases were partially accompanied by decrease in transporter LDM content. E2 increased PM content and decreased LDM content only of GLUT4 at 30 min. Insulin generally, and E2 at 20 min increased CD36 content in PM fraction. Both hormones decreased CD36 LDM content 20 min after administration. Effect of combined treatment mostly did not differ from single hormone treatment, but occasionally, particularly in distribution of GLUT4, combined treatment emphasized single hormone effect, suggesting that insulin and E2 act synergistically in regulation of energy substrate transporters in cardiac tissue.
T2  - Hormone and Metabolic Research
T1  - Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters
VL  - 43
IS  - 8
SP  - 524
EP  - 530
DO  - 10.1055/s-0031-1280784
ER  - 
@article{
author = "Tepavčević, Snežana and Korićanac, Goran and Žakula, Zorica and Milosavljević, Tijana and Stojiljković, Mojca D. and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4418",
abstract = "The estrogen binding to specific extranuclear receptors (ER) activates several intracellular pathways that are activated by insulin as well. Moreover, insulin and estradiol (E2) influence cardiac energy substrates, blood glucose and free fatty acids (FFAs), and both hormones exert cardio-beneficial effects. In view of these facts, we suggest that cross-talk between their signaling pathways might have an important role in regulation of cardiac energy substrate transport. Ovariectomized rats were treated with insulin, estradiol (E2), or their combination 20, 30, or 40 min before analysis of blood glucose and FFA level, as well as cardiac plasma membranes (PM) and low density microsomes (LDM) content of glucose (GLUT4 and GLUT1) and FFA (CD36) transporters. Insulin, given alone, or in combination with E2, decreased plasma glucose level at all time points, but did not influence FFA level, while E2 treatment itself did not change glucose and FFA concentration. Insulin increased PM GLUT4 and GLUT1 content 30 and 40 min after treatment and the increases were partially accompanied by decrease in transporter LDM content. E2 increased PM content and decreased LDM content only of GLUT4 at 30 min. Insulin generally, and E2 at 20 min increased CD36 content in PM fraction. Both hormones decreased CD36 LDM content 20 min after administration. Effect of combined treatment mostly did not differ from single hormone treatment, but occasionally, particularly in distribution of GLUT4, combined treatment emphasized single hormone effect, suggesting that insulin and E2 act synergistically in regulation of energy substrate transporters in cardiac tissue.",
journal = "Hormone and Metabolic Research",
title = "Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters",
volume = "43",
number = "8",
pages = "524-530",
doi = "10.1055/s-0031-1280784"
}
Tepavčević, S., Korićanac, G., Žakula, Z., Milosavljević, T., Stojiljković, M. D.,& Isenović, E. R. (2011). Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters.
Hormone and Metabolic Research, 43(8), 524-530.
https://doi.org/10.1055/s-0031-1280784
Tepavčević S, Korićanac G, Žakula Z, Milosavljević T, Stojiljković MD, Isenović ER. Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters. Hormone and Metabolic Research. 2011;43(8):524-530
Tepavčević Snežana, Korićanac Goran, Žakula Zorica, Milosavljević Tijana, Stojiljković Mojca D., Isenović Esma R., "Interaction Between Insulin and Estradiol in Regulation of Cardiac Glucose and Free Fatty Acid Transporters" Hormone and Metabolic Research, 43, no. 8 (2011):524-530,
https://doi.org/10.1055/s-0031-1280784 .
17
16
17

Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats

Žakula, Zorica; Korićanac, Goran; Tepavčević, Snežana; Stojiljković, Mojca D.; Milosavljević, Tijana; Isenović, Esma R.

(2011)

TY  - JOUR
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Tepavčević, Snežana
AU  - Stojiljković, Mojca D.
AU  - Milosavljević, Tijana
AU  - Isenović, Esma R.
PY  - 2011
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4494
AB  - Background Fructose consumption produces deleterious metabolic effects in animal models. The sites of fructose-induced insulin resistance are documented to be the liver, skeletal muscle, and adipose tissue, but effects of fructose-rich diet on cardiac insulin signaling and action were not investigated. Purpose and methods In order to study the potential fructose effects on development of cardiac insulin resistance, we analyzed biochemical parameters relevant for insulin action and phosphorylation of insulin signaling molecules, plasma membrane glucose transporter type 4 (GLUT4) content, and phosphorylation of endothelial nitric oxide synthase (eNOS), in ovariectomized female rats on fructose-enriched diet, in basal and insulin-stimulated conditions. Results Fructose-fed rats (FFR) had increased content of visceral adipose tissue, but not body weight. Food intake was decreased, while fluid and caloric intake were increased in FFR. Additionally, fructose diet increased plasma insulin, blood triglycerides level, and HOMA index. Stimulation of protein kinase B (Akt) signaling pathway by insulin was reduced in rats on fructose-enriched diet, but effect of fructose on extracellular signal-regulated kinase (Erk 1/2) phosphorylation was not observed. Furthermore, insulin-induced GLUT4 presence in plasma membranes of cardiac cells was decreased by fructose diet, as well as insulin stimulation of eNOS phosphorylation at Ser(1177). Conclusion In summary, these results strongly support our hypothesis that fructose diet-induced changes of plasma lipid profile and insulin sensitivity are accompanied with decrease in cardiac insulin action in ovariectomized female rats.
T2  - European Journal of Nutrition
T1  - Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats
VL  - 50
IS  - 7
SP  - 543
EP  - 551
DO  - 10.1007/s00394-010-0161-4
ER  - 
@article{
author = "Žakula, Zorica and Korićanac, Goran and Tepavčević, Snežana and Stojiljković, Mojca D. and Milosavljević, Tijana and Isenović, Esma R.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4494",
abstract = "Background Fructose consumption produces deleterious metabolic effects in animal models. The sites of fructose-induced insulin resistance are documented to be the liver, skeletal muscle, and adipose tissue, but effects of fructose-rich diet on cardiac insulin signaling and action were not investigated. Purpose and methods In order to study the potential fructose effects on development of cardiac insulin resistance, we analyzed biochemical parameters relevant for insulin action and phosphorylation of insulin signaling molecules, plasma membrane glucose transporter type 4 (GLUT4) content, and phosphorylation of endothelial nitric oxide synthase (eNOS), in ovariectomized female rats on fructose-enriched diet, in basal and insulin-stimulated conditions. Results Fructose-fed rats (FFR) had increased content of visceral adipose tissue, but not body weight. Food intake was decreased, while fluid and caloric intake were increased in FFR. Additionally, fructose diet increased plasma insulin, blood triglycerides level, and HOMA index. Stimulation of protein kinase B (Akt) signaling pathway by insulin was reduced in rats on fructose-enriched diet, but effect of fructose on extracellular signal-regulated kinase (Erk 1/2) phosphorylation was not observed. Furthermore, insulin-induced GLUT4 presence in plasma membranes of cardiac cells was decreased by fructose diet, as well as insulin stimulation of eNOS phosphorylation at Ser(1177). Conclusion In summary, these results strongly support our hypothesis that fructose diet-induced changes of plasma lipid profile and insulin sensitivity are accompanied with decrease in cardiac insulin action in ovariectomized female rats.",
journal = "European Journal of Nutrition",
title = "Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats",
volume = "50",
number = "7",
pages = "543-551",
doi = "10.1007/s00394-010-0161-4"
}
Žakula, Z., Korićanac, G., Tepavčević, S., Stojiljković, M. D., Milosavljević, T.,& Isenović, E. R. (2011). Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats.
European Journal of Nutrition, 50(7), 543-551.
https://doi.org/10.1007/s00394-010-0161-4
Žakula Z, Korićanac G, Tepavčević S, Stojiljković MD, Milosavljević T, Isenović ER. Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats. European Journal of Nutrition. 2011;50(7):543-551
Žakula Zorica, Korićanac Goran, Tepavčević Snežana, Stojiljković Mojca D., Milosavljević Tijana, Isenović Esma R., "Impairment of cardiac insulin signaling in fructose-fed ovariectomized female Wistar rats" European Journal of Nutrition, 50, no. 7 (2011):543-551,
https://doi.org/10.1007/s00394-010-0161-4 .
18
20
22

Diabetes and Antioxidants: Myth or Reality?

Haidara, Mohamed A.; Yassin, Hanaa Z.; Žakula, Zorica; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2010)

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Yassin, Hanaa Z.
AU  - Žakula, Zorica
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4112
AB  - Numerous studies have shown that increased oxidative stress (OxS) is present in diabetic patients. There is evidence that this OxS can be increased before complications associated with diabetes mellitus (DM) occur. However, the role and influence of OxS in the initiation and progression of DM remains the subject of debate. It has been suggested that in DM, OxS is caused by increased production of reactive oxygen species (ROS), and associated with reduction in antioxidant defenses and altered cellular redox status. Acute and chronic OxS which could enhance the development of complications associated with DM. This review considers recent findings on the role of antioxidants in controlling OxS and the incidence of DM with emphasis on animal and human studies.
T2  - Current Vascular Pharmacology
T1  - Diabetes and Antioxidants: Myth or Reality?
VL  - 8
IS  - 5
SP  - 661
EP  - 672
ER  - 
@article{
author = "Haidara, Mohamed A. and Yassin, Hanaa Z. and Žakula, Zorica and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4112",
abstract = "Numerous studies have shown that increased oxidative stress (OxS) is present in diabetic patients. There is evidence that this OxS can be increased before complications associated with diabetes mellitus (DM) occur. However, the role and influence of OxS in the initiation and progression of DM remains the subject of debate. It has been suggested that in DM, OxS is caused by increased production of reactive oxygen species (ROS), and associated with reduction in antioxidant defenses and altered cellular redox status. Acute and chronic OxS which could enhance the development of complications associated with DM. This review considers recent findings on the role of antioxidants in controlling OxS and the incidence of DM with emphasis on animal and human studies.",
journal = "Current Vascular Pharmacology",
title = "Diabetes and Antioxidants: Myth or Reality?",
volume = "8",
number = "5",
pages = "661-672"
}
Haidara, M. A., Yassin, H. Z., Žakula, Z., Mikhailidis, D. P.,& Isenović, E. R. (2010). Diabetes and Antioxidants: Myth or Reality?.
Current Vascular Pharmacology, 8(5), 661-672.
Haidara MA, Yassin HZ, Žakula Z, Mikhailidis DP, Isenović ER. Diabetes and Antioxidants: Myth or Reality?. Current Vascular Pharmacology. 2010;8(5):661-672
Haidara Mohamed A., Yassin Hanaa Z., Žakula Zorica, Mikhailidis Dimitri P., Isenović Esma R., "Diabetes and Antioxidants: Myth or Reality?" Current Vascular Pharmacology, 8, no. 5 (2010):661-672
19

Impact of estradiol on insulin signaling in the rat heart

Korićanac, Goran; Milosavljević, Tijana; Stojiljković, Mojca D.; Žakula, Zorica; Tepavčević, Snežana; Ribarac-Stepić, Nevena B.; Isenović, Esma R.

(2009)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
AU  - Tepavčević, Snežana
AU  - Ribarac-Stepić, Nevena B.
AU  - Isenović, Esma R.
PY  - 2009
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3648
AB  - It is well known that variation in the concentration of estrogens affects insulin action. In this study we examine the impact of estradiol (E2) on insulin signaling in the rat heart. Ovariectomized female rats were treated with E2 6 h prior to analysis of basal protein and mRNA content of insulin signaling molecules, and additionally with insulin 30 min before the experiment to delineate E2 effects on phosphorylations and molecular associations relevant for insulin signaling. The results show that E2 decreased insulin receptor (IR) tyrosine phosphorylation, while it did not alter IR protein and mRNA content. E2 administration did not chance IR substrate 1 (IRS-1) protein content and tyrosine phosphorylation, while decreased mRNA content and increased its association with the p85 subunit of phosphatidylinositol 3-kinase (PI3K). E2 decreased protein and mRNA content of IR substrate 2 (IRS-2), while did not change IRS-2 tyrosine phosphorylation and IRS-2 association with p85. The increase of IRS-1/p85 is accompanied by increase of p85 protein and mRNA levels, and by stimulation of protein kinase B (Akt) Ser(473) phosphorylation. In contrast, Akt protein and mRNA content were not changed. In summary, although in some aspects cardiac insulin signaling is obviously improved by E2 treatment (increase of p85 mRNA and protein levels, enhancement of IRS-1/p85 association and Ser(473) Akt phosphorylation), the observed decrease of IR tyrosine phosphorylation, IRS-2 protein content, and IRSs mRNA contents, suggest very complex interplay of beneficial and suppressive effects of E2, both genomic and non-genomic, in regulation of heart insulin signaling. Copyright (C) 2009 John Wiley and Sons, Ltd.
T2  - Cell Biochemistry and Function
T1  - Impact of estradiol on insulin signaling in the rat heart
VL  - 27
IS  - 2
SP  - 102
EP  - 110
DO  - 10.1002/cbf.1542
ER  - 
@article{
author = "Korićanac, Goran and Milosavljević, Tijana and Stojiljković, Mojca D. and Žakula, Zorica and Tepavčević, Snežana and Ribarac-Stepić, Nevena B. and Isenović, Esma R.",
year = "2009",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3648",
abstract = "It is well known that variation in the concentration of estrogens affects insulin action. In this study we examine the impact of estradiol (E2) on insulin signaling in the rat heart. Ovariectomized female rats were treated with E2 6 h prior to analysis of basal protein and mRNA content of insulin signaling molecules, and additionally with insulin 30 min before the experiment to delineate E2 effects on phosphorylations and molecular associations relevant for insulin signaling. The results show that E2 decreased insulin receptor (IR) tyrosine phosphorylation, while it did not alter IR protein and mRNA content. E2 administration did not chance IR substrate 1 (IRS-1) protein content and tyrosine phosphorylation, while decreased mRNA content and increased its association with the p85 subunit of phosphatidylinositol 3-kinase (PI3K). E2 decreased protein and mRNA content of IR substrate 2 (IRS-2), while did not change IRS-2 tyrosine phosphorylation and IRS-2 association with p85. The increase of IRS-1/p85 is accompanied by increase of p85 protein and mRNA levels, and by stimulation of protein kinase B (Akt) Ser(473) phosphorylation. In contrast, Akt protein and mRNA content were not changed. In summary, although in some aspects cardiac insulin signaling is obviously improved by E2 treatment (increase of p85 mRNA and protein levels, enhancement of IRS-1/p85 association and Ser(473) Akt phosphorylation), the observed decrease of IR tyrosine phosphorylation, IRS-2 protein content, and IRSs mRNA contents, suggest very complex interplay of beneficial and suppressive effects of E2, both genomic and non-genomic, in regulation of heart insulin signaling. Copyright (C) 2009 John Wiley and Sons, Ltd.",
journal = "Cell Biochemistry and Function",
title = "Impact of estradiol on insulin signaling in the rat heart",
volume = "27",
number = "2",
pages = "102-110",
doi = "10.1002/cbf.1542"
}
Korićanac, G., Milosavljević, T., Stojiljković, M. D., Žakula, Z., Tepavčević, S., Ribarac-Stepić, N. B.,& Isenović, E. R. (2009). Impact of estradiol on insulin signaling in the rat heart.
Cell Biochemistry and Function, 27(2), 102-110.
https://doi.org/10.1002/cbf.1542
Korićanac G, Milosavljević T, Stojiljković MD, Žakula Z, Tepavčević S, Ribarac-Stepić NB, Isenović ER. Impact of estradiol on insulin signaling in the rat heart. Cell Biochemistry and Function. 2009;27(2):102-110
Korićanac Goran, Milosavljević Tijana, Stojiljković Mojca D., Žakula Zorica, Tepavčević Snežana, Ribarac-Stepić Nevena B., Isenović Esma R., "Impact of estradiol on insulin signaling in the rat heart" Cell Biochemistry and Function, 27, no. 2 (2009):102-110,
https://doi.org/10.1002/cbf.1542 .
15
18
19

Effects of dexamethasone on insulin receptor in aging

Korićanac, Goran; Stojiljković, Mojca D.; Radivojša, Snežana; Žakula, Zorica; Ribarac-Stepić, Nevena B.; Isenović, Esma R.

(2008)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Stojiljković, Mojca D.
AU  - Radivojša, Snežana
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
AU  - Isenović, Esma R.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3365
AB  - The aim of this study was to examine the effects of dexamethasone (Dex) on functional properties of the rat insulin receptor (IR). Male Mill Hill hooded rats, 3, 6, 12, 18 and 21 months old, were injected with Dex (4 mg/kg) and rat liver and erythrocytes were used for experiments 18 h after Dex administration. Treatment with Dex lowered the specific binding (SB) of insulin ( INS) in the liver of 3- and 18-month-old rats and concentration of INS binding sites (N-1, N-2) and the dissociation constant of low-affinity binding sites (Kd(2)) in the liver of 6- and 18-month-old rats. In addition, Dex treatment lowered the liver IR protein level in all analyzed groups, except 21-month-old rats where it remained unchanged, but raised the IR mRNA level in 18-month-old rats. In erythrocytes, treatment with Dex decreased SB and Kd2 ( in animals 3 and 6 months old) and N1 ( in ones 3 and 18 months old). Following Dex treatment, the INS plasma level increased ( in rats 3, 18 and 21 months old), while glucose (Glu) concentration increased in 3 and 12 months old, but decreased in 6- and 21-month-old rats. In summary, Dex exerts the strongest effect on the erythrocyte IR of 3- and 6- month-old rats and the hepatic IR of 18-month-old rats. IR in both tissues is almost insensitive to Dex in 12- and 21-month-old rats. The pattern of age-related changes of IR induced by Dex does not correlate with changes of plasma Glu and INS.
T2  - Acta Biologica Hungarica
T1  - Effects of dexamethasone on insulin receptor in aging
VL  - 59
IS  - 1
SP  - 17
EP  - 29
DO  - 10.1556/ABiol.59.2008.1.2
ER  - 
@article{
author = "Korićanac, Goran and Stojiljković, Mojca D. and Radivojša, Snežana and Žakula, Zorica and Ribarac-Stepić, Nevena B. and Isenović, Esma R.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3365",
abstract = "The aim of this study was to examine the effects of dexamethasone (Dex) on functional properties of the rat insulin receptor (IR). Male Mill Hill hooded rats, 3, 6, 12, 18 and 21 months old, were injected with Dex (4 mg/kg) and rat liver and erythrocytes were used for experiments 18 h after Dex administration. Treatment with Dex lowered the specific binding (SB) of insulin ( INS) in the liver of 3- and 18-month-old rats and concentration of INS binding sites (N-1, N-2) and the dissociation constant of low-affinity binding sites (Kd(2)) in the liver of 6- and 18-month-old rats. In addition, Dex treatment lowered the liver IR protein level in all analyzed groups, except 21-month-old rats where it remained unchanged, but raised the IR mRNA level in 18-month-old rats. In erythrocytes, treatment with Dex decreased SB and Kd2 ( in animals 3 and 6 months old) and N1 ( in ones 3 and 18 months old). Following Dex treatment, the INS plasma level increased ( in rats 3, 18 and 21 months old), while glucose (Glu) concentration increased in 3 and 12 months old, but decreased in 6- and 21-month-old rats. In summary, Dex exerts the strongest effect on the erythrocyte IR of 3- and 6- month-old rats and the hepatic IR of 18-month-old rats. IR in both tissues is almost insensitive to Dex in 12- and 21-month-old rats. The pattern of age-related changes of IR induced by Dex does not correlate with changes of plasma Glu and INS.",
journal = "Acta Biologica Hungarica",
title = "Effects of dexamethasone on insulin receptor in aging",
volume = "59",
number = "1",
pages = "17-29",
doi = "10.1556/ABiol.59.2008.1.2"
}
Korićanac, G., Stojiljković, M. D., Radivojša, S., Žakula, Z., Ribarac-Stepić, N. B.,& Isenović, E. R. (2008). Effects of dexamethasone on insulin receptor in aging.
Acta Biologica Hungarica, 59(1), 17-29.
https://doi.org/10.1556/ABiol.59.2008.1.2
Korićanac G, Stojiljković MD, Radivojša S, Žakula Z, Ribarac-Stepić NB, Isenović ER. Effects of dexamethasone on insulin receptor in aging. Acta Biologica Hungarica. 2008;59(1):17-29
Korićanac Goran, Stojiljković Mojca D., Radivojša Snežana, Žakula Zorica, Ribarac-Stepić Nevena B., Isenović Esma R., "Effects of dexamethasone on insulin receptor in aging" Acta Biologica Hungarica, 59, no. 1 (2008):17-29,
https://doi.org/10.1556/ABiol.59.2008.1.2 .
2
2
2

Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol

Korićanac, Goran; Milosavljević, Tijana; Stojiljković, Mojca D.; Žakula, Zorica; Ribarac-Stepić, Nevena B.; Isenović, Esma R.

(2008)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Milosavljević, Tijana
AU  - Stojiljković, Mojca D.
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
AU  - Isenović, Esma R.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3378
AB  - We used rat hepatic and uterine tissues to examine the impact of estradiol (E2) on insulin (INS) signaling. Ovariectotnized (OVX) female Wistar rats were treated with E2 (20 mu g/kg b.wt., i.p.) and used for the experiment 6 h after E2 administration. To highlight E2 effects on tyrosine phosphorylation of INS receptor (IR) and INS receptor substrates (IRSs) and IRSs association with p85 subunit of phosphatidylinositol 3-kinase (PI3-K) in the context of INS signaling, E2-treated OVX rats were also injected with INS (20 IU, i.p.), 30 min before the experiment. Treatment with E2 did not change the levels of plasma INS and glucose (Glu). However, it significantly decreased the free fatty acid (FFA) level and increased uterine weight. Furthermore, the results show that E2 had no effect on the content of hepatic IR protein, but significantly increased IR protein content in the uterus and decreased IR tyrosine phosphorylation in both the liver and uterus. Compared to the control, hepatic IRS-1 and IRS-2 were significantly decreased and increased, respectively, after E2 treatment. Protein content of both molecules, IRS-1 and IRS-2, was increased in uterine tissue after E2 administration. Protein content of the p85 subunit of PI3-K and that of protein kinase B (Akt) were increased in the uterus, with no changes in the liver. The results suggest that E2 treatment induces tissue-specific changes in INS signaling. The consequences of E2 treatment on INS signaling molecules are more apparent in the uterus, but their physiological relevance for INS action is probably greater in the liver. (c) 2007 Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol
VL  - 108
IS  - 1-2
SP  - 109
EP  - 116
DO  - 10.1016/j.jsbmb.2007.06.001
ER  - 
@article{
author = "Korićanac, Goran and Milosavljević, Tijana and Stojiljković, Mojca D. and Žakula, Zorica and Ribarac-Stepić, Nevena B. and Isenović, Esma R.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3378",
abstract = "We used rat hepatic and uterine tissues to examine the impact of estradiol (E2) on insulin (INS) signaling. Ovariectotnized (OVX) female Wistar rats were treated with E2 (20 mu g/kg b.wt., i.p.) and used for the experiment 6 h after E2 administration. To highlight E2 effects on tyrosine phosphorylation of INS receptor (IR) and INS receptor substrates (IRSs) and IRSs association with p85 subunit of phosphatidylinositol 3-kinase (PI3-K) in the context of INS signaling, E2-treated OVX rats were also injected with INS (20 IU, i.p.), 30 min before the experiment. Treatment with E2 did not change the levels of plasma INS and glucose (Glu). However, it significantly decreased the free fatty acid (FFA) level and increased uterine weight. Furthermore, the results show that E2 had no effect on the content of hepatic IR protein, but significantly increased IR protein content in the uterus and decreased IR tyrosine phosphorylation in both the liver and uterus. Compared to the control, hepatic IRS-1 and IRS-2 were significantly decreased and increased, respectively, after E2 treatment. Protein content of both molecules, IRS-1 and IRS-2, was increased in uterine tissue after E2 administration. Protein content of the p85 subunit of PI3-K and that of protein kinase B (Akt) were increased in the uterus, with no changes in the liver. The results suggest that E2 treatment induces tissue-specific changes in INS signaling. The consequences of E2 treatment on INS signaling molecules are more apparent in the uterus, but their physiological relevance for INS action is probably greater in the liver. (c) 2007 Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol",
volume = "108",
number = "1-2",
pages = "109-116",
doi = "10.1016/j.jsbmb.2007.06.001"
}
Korićanac, G., Milosavljević, T., Stojiljković, M. D., Žakula, Z., Ribarac-Stepić, N. B.,& Isenović, E. R. (2008). Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol.
Journal of Steroid Biochemistry and Molecular Biology, 108(1-2), 109-116.
https://doi.org/10.1016/j.jsbmb.2007.06.001
Korićanac G, Milosavljević T, Stojiljković MD, Žakula Z, Ribarac-Stepić NB, Isenović ER. Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol. Journal of Steroid Biochemistry and Molecular Biology. 2008;108(1-2):109-116
Korićanac Goran, Milosavljević Tijana, Stojiljković Mojca D., Žakula Zorica, Ribarac-Stepić Nevena B., Isenović Esma R., "Insulin signaling in the liver and uterus of ovariectomized rats treated with estradiol" Journal of Steroid Biochemistry and Molecular Biology, 108, no. 1-2 (2008):109-116,
https://doi.org/10.1016/j.jsbmb.2007.06.001 .
15
16
17

Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin

Isenović, Esma R.; Žakula, Zorica; Korićanac, Goran; Ribarac-Stepić, Nevena B.

(2008)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Ribarac-Stepić, Nevena B.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3422
AB  - This investigation addresses the interaction of insulin (INS) and glucocorticoid (GC) signaling in the hepatic regulation of tryptophan oxygenase (TO) enzyme activity in the rat. Male Wistar rats (200-250 g b.w) received an injection of the different doses of INS (10, 25, 50, 70 and 100 pg/200 g b.w., i.p.) and were used for experiments 3 h and 18 h after INS administration. This study shows that maximum of TO activity was found at dose of 50 mu g of INS with peak increases observed at 3 h and 18 h after injection of INS, while INS had no effect on TO activity in adrenalectomized rats. The analysis of INS effects on glucocorticoid receptor-complex (GC/GR complex) stability shows that complexes from INS-treated rats are less stable than those from control animals. In addition, INS-stimulated stability of glucocorticoid receptor (GR) protein was significantly increased from the controls. Furthermore, the results show that GC/GR complexes from INS-treated rats could be activated and accumulated at higher rate in cell nuclei of control animals. These data support the involvement of INS in modulation of GC signaling pathway which mediates, in part, the activity of TO.
T2  - Physiological Research
T1  - Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin
VL  - 57
IS  - 1
SP  - 101
EP  - 107
ER  - 
@article{
author = "Isenović, Esma R. and Žakula, Zorica and Korićanac, Goran and Ribarac-Stepić, Nevena B.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3422",
abstract = "This investigation addresses the interaction of insulin (INS) and glucocorticoid (GC) signaling in the hepatic regulation of tryptophan oxygenase (TO) enzyme activity in the rat. Male Wistar rats (200-250 g b.w) received an injection of the different doses of INS (10, 25, 50, 70 and 100 pg/200 g b.w., i.p.) and were used for experiments 3 h and 18 h after INS administration. This study shows that maximum of TO activity was found at dose of 50 mu g of INS with peak increases observed at 3 h and 18 h after injection of INS, while INS had no effect on TO activity in adrenalectomized rats. The analysis of INS effects on glucocorticoid receptor-complex (GC/GR complex) stability shows that complexes from INS-treated rats are less stable than those from control animals. In addition, INS-stimulated stability of glucocorticoid receptor (GR) protein was significantly increased from the controls. Furthermore, the results show that GC/GR complexes from INS-treated rats could be activated and accumulated at higher rate in cell nuclei of control animals. These data support the involvement of INS in modulation of GC signaling pathway which mediates, in part, the activity of TO.",
journal = "Physiological Research",
title = "Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin",
volume = "57",
number = "1",
pages = "101-107"
}
Isenović, E. R., Žakula, Z., Korićanac, G.,& Ribarac-Stepić, N. B. (2008). Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin.
Physiological Research, 57(1), 101-107.
Isenović ER, Žakula Z, Korićanac G, Ribarac-Stepić NB. Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin. Physiological Research. 2008;57(1):101-107
Isenović Esma R., Žakula Zorica, Korićanac Goran, Ribarac-Stepić Nevena B., "Comparative analysis of tryptophan oxygenase activity and glucocorticoid receptor under the influence of insulin" Physiological Research, 57, no. 1 (2008):101-107
1

Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension

Sudar, Emina; Velebit, Mena; Gluvić, Zoran; Žakula, Zorica; Lazic, Emilija; Vuksanovic-Topic, Ljiljana; Putnikovic, Biljana; Neskovic, Aleksandar; Isenović, Esma R.

(2008)

TY  - JOUR
AU  - Sudar, Emina
AU  - Velebit, Mena
AU  - Gluvić, Zoran
AU  - Žakula, Zorica
AU  - Lazic, Emilija
AU  - Vuksanovic-Topic, Ljiljana
AU  - Putnikovic, Biljana
AU  - Neskovic, Aleksandar
AU  - Isenović, Esma R.
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3442
AB  - Causal relationship between sodium and hypertension has been proposed and various changes in Na+, K+-ATPase (sodium pump) activity have been described in established primary hypertension. A number of direct vascular effects of estradiol have been reported, including its impact on the regulation of sodium pump activity and vasomotor tone. The effects of estradiol involve the activation of multiple signaling cascades, including phosphatydil inositol-3 kinase (PI3K) and p42/44 mitogen-activated protein kinase (p42/44 MAPK). In addition, some of the effects of estradiol have been linked to activity of cytosolic phospholipase A(2) (cPLA(2)). One possible cardioprotective mechanism of estradiol involves of the interaction between estradiol and the rennin-angiotensin system (RAS). Elevated circulating and tissue levels of angiotensin II (Ang II) have been implicated in the development of hypertension and heart failure. The aim of our investigation was to elucidate the signaling mechanisms employed by estradiol and Ang II in mediating sodium pump, in vascular smooth muscle cells (VSMC). The aim of our investigation was to elucidate the signaling mechanisms employed by estradiol and Ang II in mediating sodium pump activity/expression in VSMC, with particular emphasis on PI3K/cPLA(2)/p42/44(MAPK) signaling pathways. Our primary hypothesis is that estradiol stimulates sodium. pump activity/expression in VSMC via PI3K/cPLA(2)/p42/44(MAPK) dependent mechanism and, that impaired estradiol-stimulated sodium pump activity/expression in hypertensive rodent models (i.e. SHR), Ang II-mediated vascular impairment of estradiol is related to a decrease ability of estradiol to stimulate the PI3K/cPLA(2)/p42/44(MAPK) signaling pathways. An important corollary to this hypothesis is that in hypertensive state (i.e. SHR rats) the decreasing in ACE enzyme activity and/or AT1 receptor expression caused by administration of estradiol is accompanying with abrogated ability of Ang 11 to decrease IRS-1/PI3K association, and consequent PI3K/cPLA(2)/p42/44(MAPK) activity and associated sodium pump activity/expression. A clear characterization of how Ang II attenuates estradiol signaling may lead to a better understanding of the molecular mechanism(s) underlying pathophysiological conditions such as hypertension and to understanding how certain pathophysiological situations affect sodium pump activity/expression in VSMC. (c) 2008 Elsevier Ltd. All rights reserved.
T2  - Journal of Theoretical Biology
T1  - Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension
VL  - 251
IS  - 4
SP  - 584
EP  - 592
DO  - 10.1016/j.jtbi.2007.12.023
ER  - 
@article{
author = "Sudar, Emina and Velebit, Mena and Gluvić, Zoran and Žakula, Zorica and Lazic, Emilija and Vuksanovic-Topic, Ljiljana and Putnikovic, Biljana and Neskovic, Aleksandar and Isenović, Esma R.",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3442",
abstract = "Causal relationship between sodium and hypertension has been proposed and various changes in Na+, K+-ATPase (sodium pump) activity have been described in established primary hypertension. A number of direct vascular effects of estradiol have been reported, including its impact on the regulation of sodium pump activity and vasomotor tone. The effects of estradiol involve the activation of multiple signaling cascades, including phosphatydil inositol-3 kinase (PI3K) and p42/44 mitogen-activated protein kinase (p42/44 MAPK). In addition, some of the effects of estradiol have been linked to activity of cytosolic phospholipase A(2) (cPLA(2)). One possible cardioprotective mechanism of estradiol involves of the interaction between estradiol and the rennin-angiotensin system (RAS). Elevated circulating and tissue levels of angiotensin II (Ang II) have been implicated in the development of hypertension and heart failure. The aim of our investigation was to elucidate the signaling mechanisms employed by estradiol and Ang II in mediating sodium pump, in vascular smooth muscle cells (VSMC). The aim of our investigation was to elucidate the signaling mechanisms employed by estradiol and Ang II in mediating sodium pump activity/expression in VSMC, with particular emphasis on PI3K/cPLA(2)/p42/44(MAPK) signaling pathways. Our primary hypothesis is that estradiol stimulates sodium. pump activity/expression in VSMC via PI3K/cPLA(2)/p42/44(MAPK) dependent mechanism and, that impaired estradiol-stimulated sodium pump activity/expression in hypertensive rodent models (i.e. SHR), Ang II-mediated vascular impairment of estradiol is related to a decrease ability of estradiol to stimulate the PI3K/cPLA(2)/p42/44(MAPK) signaling pathways. An important corollary to this hypothesis is that in hypertensive state (i.e. SHR rats) the decreasing in ACE enzyme activity and/or AT1 receptor expression caused by administration of estradiol is accompanying with abrogated ability of Ang 11 to decrease IRS-1/PI3K association, and consequent PI3K/cPLA(2)/p42/44(MAPK) activity and associated sodium pump activity/expression. A clear characterization of how Ang II attenuates estradiol signaling may lead to a better understanding of the molecular mechanism(s) underlying pathophysiological conditions such as hypertension and to understanding how certain pathophysiological situations affect sodium pump activity/expression in VSMC. (c) 2008 Elsevier Ltd. All rights reserved.",
journal = "Journal of Theoretical Biology",
title = "Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension",
volume = "251",
number = "4",
pages = "584-592",
doi = "10.1016/j.jtbi.2007.12.023"
}
Sudar, E., Velebit, M., Gluvić, Z., Žakula, Z., Lazic, E., Vuksanovic-Topic, L., Putnikovic, B., Neskovic, A.,& Isenović, E. R. (2008). Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension.
Journal of Theoretical Biology, 251(4), 584-592.
https://doi.org/10.1016/j.jtbi.2007.12.023
Sudar E, Velebit M, Gluvić Z, Žakula Z, Lazic E, Vuksanovic-Topic L, Putnikovic B, Neskovic A, Isenović ER. Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension. Journal of Theoretical Biology. 2008;251(4):584-592
Sudar Emina, Velebit Mena, Gluvić Zoran, Žakula Zorica, Lazic Emilija, Vuksanovic-Topic Ljiljana, Putnikovic Biljana, Neskovic Aleksandar, Isenović Esma R., "Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension" Journal of Theoretical Biology, 251, no. 4 (2008):584-592,
https://doi.org/10.1016/j.jtbi.2007.12.023 .
18
23
28

Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy

Isenović, Esma R.; Trpković, Andreja; Žakula, Zorica; Korićanac, Goran; Marche, Pierre

(2008)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Trpković, Andreja
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Marche, Pierre
PY  - 2008
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7803
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.
T2  - Current Hypertension Reviews
T1  - Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy
VL  - 4
IS  - 3
SP  - 190
EP  - 196
DO  - 10.2174/157340208785132590
ER  - 
@article{
author = "Isenović, Esma R. and Trpković, Andreja and Žakula, Zorica and Korićanac, Goran and Marche, Pierre",
year = "2008",
url = "http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190, http://vinar.vin.bg.ac.rs/handle/123456789/7803",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.",
journal = "Current Hypertension Reviews",
title = "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy",
volume = "4",
number = "3",
pages = "190-196",
doi = "10.2174/157340208785132590"
}
Isenović, E. R., Trpković, A., Žakula, Z., Korićanac, G.,& Marche, P. (2008). Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy.
Current Hypertension Reviews, 4(3), 190-196.
https://doi.org/10.2174/157340208785132590
Isenović ER, Trpković A, Žakula Z, Korićanac G, Marche P. Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy. Current Hypertension Reviews. 2008;4(3):190-196
Isenović Esma R., Trpković Andreja, Žakula Zorica, Korićanac Goran, Marche Pierre, "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy" Current Hypertension Reviews, 4, no. 3 (2008):190-196,
https://doi.org/10.2174/157340208785132590 .
3
5

Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy

Isenović, Esma R.; Trpković, Andreja; Žakula, Zorica; Korićanac, Goran; Marche, Pierre

(2008)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Trpković, Andreja
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Marche, Pierre
PY  - 2008
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7837
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review. © 2008 Bentham Science Publishers Ltd.
T2  - Current Hypertension Reviews
T1  - Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy
VL  - 4
IS  - 3
SP  - 190
EP  - 196
DO  - 10.2174/157340208785132590
ER  - 
@article{
author = "Isenović, Esma R. and Trpković, Andreja and Žakula, Zorica and Korićanac, Goran and Marche, Pierre",
year = "2008",
url = "http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190, http://vinar.vin.bg.ac.rs/handle/123456789/7837",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review. © 2008 Bentham Science Publishers Ltd.",
journal = "Current Hypertension Reviews",
title = "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy",
volume = "4",
number = "3",
pages = "190-196",
doi = "10.2174/157340208785132590"
}
Isenović, E. R., Trpković, A., Žakula, Z., Korićanac, G.,& Marche, P. (2008). Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy.
Current Hypertension Reviews, 4(3), 190-196.
https://doi.org/10.2174/157340208785132590
Isenović ER, Trpković A, Žakula Z, Korićanac G, Marche P. Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy. Current Hypertension Reviews. 2008;4(3):190-196
Isenović Esma R., Trpković Andreja, Žakula Zorica, Korićanac Goran, Marche Pierre, "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy" Current Hypertension Reviews, 4, no. 3 (2008):190-196,
https://doi.org/10.2174/157340208785132590 .
3
5

Regulation of the inducible nitric oxide synthase and sodium pump in type 1 diabetes

Žakula, Zorica; Korićanac, Goran; Putnikovic, Biljana; Markovic, Ljiljana; Isenović, Esma R.

(2007)

TY  - JOUR
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Putnikovic, Biljana
AU  - Markovic, Ljiljana
AU  - Isenović, Esma R.
PY  - 2007
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3205
AB  - Insulin-like growth factor-1 (IGF-1) is a hormone and growth factor closely related to insulin. The autocrine/paracrine actions of IGF-1 involve activation of inducible nitric oxide synthase (iNOS) and the Na(+), K(+)-ATPase sodium pump in cardiovascular tissues. Data from literature indicate that iNOS is expressed in vascular smooth muscle cells (VSMC) and that IGF- 1 -induced release of NO is both rapid and delayed. We hypothesize that impaired IGF-1 -induced sodium pump activity/ expression in rats with type 1 diabetes is related to activation of phosphatidytinositol 3 kinase (PI3K)/cytosolic phospholipase 2 (cPLA(2))/protein kinase B (Akt) signaling, and that IGF-1 prevents acute and chronic dysfunction of iNOS and sodium pump activity in a chemically induced model of type 1 diabetes, the streptozotocin -treated rat heart (STZ). Understanding how iNOS and sodium pump activity are regulated by IGF-1 activation of the PI3K/cPLA(2)/Akt cascade should provide novel and fundamental knowledge regarding the regulatory actions of IGF-1 in promoting vasodilation. Since insulin resistance is currently a major focus of research, the use of IGF-1 to improve insulin resistance and glucose metabolism has opened a new arena for treatment of comorbid conditions. Future investigations should now focus on mechanisms of action of IGF-1 and its clinical applicability. (c) 2007 Elsevier Ltd. All rights reserved.
T2  - Medical Hypotheses
T1  - Regulation of the inducible nitric oxide synthase and sodium pump in type 1 diabetes
VL  - 69
IS  - 2
SP  - 302
EP  - 306
DO  - 10.1016/j.mehy.2006.11.045
ER  - 
@article{
author = "Žakula, Zorica and Korićanac, Goran and Putnikovic, Biljana and Markovic, Ljiljana and Isenović, Esma R.",
year = "2007",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3205",
abstract = "Insulin-like growth factor-1 (IGF-1) is a hormone and growth factor closely related to insulin. The autocrine/paracrine actions of IGF-1 involve activation of inducible nitric oxide synthase (iNOS) and the Na(+), K(+)-ATPase sodium pump in cardiovascular tissues. Data from literature indicate that iNOS is expressed in vascular smooth muscle cells (VSMC) and that IGF- 1 -induced release of NO is both rapid and delayed. We hypothesize that impaired IGF-1 -induced sodium pump activity/ expression in rats with type 1 diabetes is related to activation of phosphatidytinositol 3 kinase (PI3K)/cytosolic phospholipase 2 (cPLA(2))/protein kinase B (Akt) signaling, and that IGF-1 prevents acute and chronic dysfunction of iNOS and sodium pump activity in a chemically induced model of type 1 diabetes, the streptozotocin -treated rat heart (STZ). Understanding how iNOS and sodium pump activity are regulated by IGF-1 activation of the PI3K/cPLA(2)/Akt cascade should provide novel and fundamental knowledge regarding the regulatory actions of IGF-1 in promoting vasodilation. Since insulin resistance is currently a major focus of research, the use of IGF-1 to improve insulin resistance and glucose metabolism has opened a new arena for treatment of comorbid conditions. Future investigations should now focus on mechanisms of action of IGF-1 and its clinical applicability. (c) 2007 Elsevier Ltd. All rights reserved.",
journal = "Medical Hypotheses",
title = "Regulation of the inducible nitric oxide synthase and sodium pump in type 1 diabetes",
volume = "69",
number = "2",
pages = "302-306",
doi = "10.1016/j.mehy.2006.11.045"
}
Žakula, Z., Korićanac, G., Putnikovic, B., Markovic, L.,& Isenović, E. R. (2007). Regulation of the inducible nitric oxide synthase and sodium pump in type 1 diabetes.
Medical Hypotheses, 69(2), 302-306.
https://doi.org/10.1016/j.mehy.2006.11.045
Žakula Z, Korićanac G, Putnikovic B, Markovic L, Isenović ER. Regulation of the inducible nitric oxide synthase and sodium pump in type 1 diabetes. Medical Hypotheses. 2007;69(2):302-306
Žakula Zorica, Korićanac Goran, Putnikovic Biljana, Markovic Ljiljana, Isenović Esma R., "Regulation of the inducible nitric oxide synthase and sodium pump in type 1 diabetes" Medical Hypotheses, 69, no. 2 (2007):302-306,
https://doi.org/10.1016/j.mehy.2006.11.045 .
3
6
8
11

Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor

Žakula, Zorica; Isenović, Esma R.; Stojiljković, Mojca D.; Tepavčević, Snežana; Ribarac-Stepić, Nevena B.

(2007)

TY  - JOUR
AU  - Žakula, Zorica
AU  - Isenović, Esma R.
AU  - Stojiljković, Mojca D.
AU  - Tepavčević, Snežana
AU  - Ribarac-Stepić, Nevena B.
PY  - 2007
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3412
AB  - The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.
T2  - Archives of biological sciences
T1  - Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor
VL  - 59
IS  - 2
SP  - 105
EP  - 112
DO  - 10.2298/ABS0702105Z
ER  - 
@article{
author = "Žakula, Zorica and Isenović, Esma R. and Stojiljković, Mojca D. and Tepavčević, Snežana and Ribarac-Stepić, Nevena B.",
year = "2007",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3412",
abstract = "The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.",
journal = "Archives of biological sciences",
title = "Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor",
volume = "59",
number = "2",
pages = "105-112",
doi = "10.2298/ABS0702105Z"
}
Žakula, Z., Isenović, E. R., Stojiljković, M. D., Tepavčević, S.,& Ribarac-Stepić, N. B. (2007). Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor.
Archives of biological sciences, 59(2), 105-112.
https://doi.org/10.2298/ABS0702105Z
Žakula Z, Isenović ER, Stojiljković MD, Tepavčević S, Ribarac-Stepić NB. Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor. Archives of biological sciences. 2007;59(2):105-112
Žakula Zorica, Isenović Esma R., Stojiljković Mojca D., Tepavčević Snežana, Ribarac-Stepić Nevena B., "Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor" Archives of biological sciences, 59, no. 2 (2007):105-112,
https://doi.org/10.2298/ABS0702105Z .

Insulin modulates rat liver glucocorticoid receptor

Isenović, Esma R.; Žakula, Zorica; Korićanac, Goran; Ribarac-Stepić, Nevena B.

(2006)

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Ribarac-Stepić, Nevena B.
PY  - 2006
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/2982
AB  - This investigation used cytosol fraction of rat liver to examine the effects of insulin ( INS) on functional properties of glucocorticoid receptor ( GR). Male Wistar rats ( 220 - 250 g b.wt.) were injected with INS ( 50 mu g/200 g b.wt, i.p.) and 18 h after INS administration used for experiments. INS-stimulated dissociation of G-R complexes was significantly increased by 133% compared to control level. However, INS treatment significantly stimulated stability of GR protein by 138% above control value. Furthermore, results show that INS stimulated activation of formed cytosol [ H-3] TA-R complexes by 143% in respect to control. [ H-3] TA-R complexes from INS treated animals could be activated and accumulated at higher rate in cell nuclei of control animals. The physiological relevance of the data was confirmed by INS-related stimulation of Tryptophan oxigenase ( TO) activity. It was observed that INS stimulated TO activity while INS injected to adrenalectomized rats, exhibited less effects compared to control. The results indicate that a glucocorticoid hormone ( CORT) enhances INS induced stimulation of TO activity, as evidenced by enhanced enzyme activity. Presented data suggest: that INS treatment leads to modifications of the GR protein and the nuclear components and that INS activates the rat liver CORT signaling pathway which mediates, in part, the activity of TO.
T2  - Acta Biologica Hungarica
T1  - Insulin modulates rat liver glucocorticoid receptor
VL  - 57
IS  - 1
SP  - 37
EP  - 48
DO  - 10.1556/ABiol.57.2006.1.4
ER  - 
@article{
author = "Isenović, Esma R. and Žakula, Zorica and Korićanac, Goran and Ribarac-Stepić, Nevena B.",
year = "2006",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/2982",
abstract = "This investigation used cytosol fraction of rat liver to examine the effects of insulin ( INS) on functional properties of glucocorticoid receptor ( GR). Male Wistar rats ( 220 - 250 g b.wt.) were injected with INS ( 50 mu g/200 g b.wt, i.p.) and 18 h after INS administration used for experiments. INS-stimulated dissociation of G-R complexes was significantly increased by 133% compared to control level. However, INS treatment significantly stimulated stability of GR protein by 138% above control value. Furthermore, results show that INS stimulated activation of formed cytosol [ H-3] TA-R complexes by 143% in respect to control. [ H-3] TA-R complexes from INS treated animals could be activated and accumulated at higher rate in cell nuclei of control animals. The physiological relevance of the data was confirmed by INS-related stimulation of Tryptophan oxigenase ( TO) activity. It was observed that INS stimulated TO activity while INS injected to adrenalectomized rats, exhibited less effects compared to control. The results indicate that a glucocorticoid hormone ( CORT) enhances INS induced stimulation of TO activity, as evidenced by enhanced enzyme activity. Presented data suggest: that INS treatment leads to modifications of the GR protein and the nuclear components and that INS activates the rat liver CORT signaling pathway which mediates, in part, the activity of TO.",
journal = "Acta Biologica Hungarica",
title = "Insulin modulates rat liver glucocorticoid receptor",
volume = "57",
number = "1",
pages = "37-48",
doi = "10.1556/ABiol.57.2006.1.4"
}
Isenović, E. R., Žakula, Z., Korićanac, G.,& Ribarac-Stepić, N. B. (2006). Insulin modulates rat liver glucocorticoid receptor.
Acta Biologica Hungarica, 57(1), 37-48.
https://doi.org/10.1556/ABiol.57.2006.1.4
Isenović ER, Žakula Z, Korićanac G, Ribarac-Stepić NB. Insulin modulates rat liver glucocorticoid receptor. Acta Biologica Hungarica. 2006;57(1):37-48
Isenović Esma R., Žakula Zorica, Korićanac Goran, Ribarac-Stepić Nevena B., "Insulin modulates rat liver glucocorticoid receptor" Acta Biologica Hungarica, 57, no. 1 (2006):37-48,
https://doi.org/10.1556/ABiol.57.2006.1.4 .
3
3
2

The influence of 17-oxo- and 17-hydroxy-16,17-secoestratriene derivatives on estrogen receptor

Jovanovic-Santa, S; Petrović, Julijana; Sakac, M; Žakula, Zorica; Isenović, Esma R.; Ribarac-Stepić, Nevena B.

(2006)

TY  - JOUR
AU  - Jovanovic-Santa, S
AU  - Petrović, Julijana
AU  - Sakac, M
AU  - Žakula, Zorica
AU  - Isenović, Esma R.
AU  - Ribarac-Stepić, Nevena B.
PY  - 2006
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3007
AB  - Since many of newly synthesised D-secoestratriene derivatives showed antiestrogenic effect, with almost a total loss of estrogenic activity, we studied the effects of some of these compounds on estrogen receptors (ER), the translocation of the estrogen-ER complexes formed in presence of competing substances into the nucleus, as well as the binding of these complexes to DNA. The results of uterotrophic effects of analysed derivatives are in agreement with the influence of these compounds on activity and binding parameters of estrogen receptors. Namely, compounds that show relatively high antiestrogenic activity predominantly increase K-d and inhibit translocation to nuclei of radioactive complexes formed in their presence. On the other hand, compounds that do not significantly change binding parameters of estrogen receptors do not show antiestrogenic effect in in vivo experiments.
T2  - Collection of Czechoslovak Chemical Communications
T1  - The influence of 17-oxo- and 17-hydroxy-16,17-secoestratriene derivatives on estrogen receptor
VL  - 71
IS  - 4
SP  - 532
EP  - 542
DO  - 10.1135/cccc20060532
ER  - 
@article{
author = "Jovanovic-Santa, S and Petrović, Julijana and Sakac, M and Žakula, Zorica and Isenović, Esma R. and Ribarac-Stepić, Nevena B.",
year = "2006",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3007",
abstract = "Since many of newly synthesised D-secoestratriene derivatives showed antiestrogenic effect, with almost a total loss of estrogenic activity, we studied the effects of some of these compounds on estrogen receptors (ER), the translocation of the estrogen-ER complexes formed in presence of competing substances into the nucleus, as well as the binding of these complexes to DNA. The results of uterotrophic effects of analysed derivatives are in agreement with the influence of these compounds on activity and binding parameters of estrogen receptors. Namely, compounds that show relatively high antiestrogenic activity predominantly increase K-d and inhibit translocation to nuclei of radioactive complexes formed in their presence. On the other hand, compounds that do not significantly change binding parameters of estrogen receptors do not show antiestrogenic effect in in vivo experiments.",
journal = "Collection of Czechoslovak Chemical Communications",
title = "The influence of 17-oxo- and 17-hydroxy-16,17-secoestratriene derivatives on estrogen receptor",
volume = "71",
number = "4",
pages = "532-542",
doi = "10.1135/cccc20060532"
}
Jovanovic-Santa, S., Petrović, J., Sakac, M., Žakula, Z., Isenović, E. R.,& Ribarac-Stepić, N. B. (2006). The influence of 17-oxo- and 17-hydroxy-16,17-secoestratriene derivatives on estrogen receptor.
Collection of Czechoslovak Chemical Communications, 71(4), 532-542.
https://doi.org/10.1135/cccc20060532
Jovanovic-Santa S, Petrović J, Sakac M, Žakula Z, Isenović ER, Ribarac-Stepić NB. The influence of 17-oxo- and 17-hydroxy-16,17-secoestratriene derivatives on estrogen receptor. Collection of Czechoslovak Chemical Communications. 2006;71(4):532-542
Jovanovic-Santa S, Petrović Julijana, Sakac M, Žakula Zorica, Isenović Esma R., Ribarac-Stepić Nevena B., "The influence of 17-oxo- and 17-hydroxy-16,17-secoestratriene derivatives on estrogen receptor" Collection of Czechoslovak Chemical Communications, 71, no. 4 (2006):532-542,
https://doi.org/10.1135/cccc20060532 .
3
4
4

Time dependent effects of dexamethasone on serum insulin level and insulin receptors in rat liver and erythrocytes

Korićanac, Goran; Isenović, Esma R.; Stojanovic-Susulic, V; Miskovic, D; Žakula, Zorica; Ribarac-Stepić, Nevena B.

(2006)

TY  - JOUR
AU  - Korićanac, Goran
AU  - Isenović, Esma R.
AU  - Stojanovic-Susulic, V
AU  - Miskovic, D
AU  - Žakula, Zorica
AU  - Ribarac-Stepić, Nevena B.
PY  - 2006
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3023
AB  - The effects of glucocorticoid excess on regulation of insulin receptors were investigated in dexamethasone-treated rats. Glucocorticoid excess was produced by administration of dexamethasone (0.5 mg/100 g b.w.) 30 min, 4, 12, 18, 24, 42 or 70 h before experiments. This treatment caused time-dependent changes of glucose and insulin concentration in blood, as well as in amounts of specific insulin binding and insulin receptors of liver cells and erythrocytes. The time intervals in which dexamethasone produced the increase in insulin concentration were accompanied with decrease in insulin binding to receptors in membranes of liver cells, while significant changes in insulin binding to receptors of erythrocytes were not observed under the same experimental conditions. The effect is maximal 18 and 42 h after dexamethasone treatment that increase insulin blood level by about 85% and 60%, respectively. Receptor analysis revealed that changes in specific binding of insulin could be due to significant changes in amount of binding sites on cell surface rather than to mild alteration in receptor affinity. These findings suggest that besides the changes in insulin level, the alterations in insulin receptor number and affinity may play a major role in the states of altered insulin sensitivity which accompany glucocorticoid excess.
T2  - General Physiology and Biophysics
T1  - Time dependent effects of dexamethasone on serum insulin level and insulin receptors in rat liver and erythrocytes
VL  - 25
IS  - 1
SP  - 11
EP  - 24
ER  - 
@article{
author = "Korićanac, Goran and Isenović, Esma R. and Stojanovic-Susulic, V and Miskovic, D and Žakula, Zorica and Ribarac-Stepić, Nevena B.",
year = "2006",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3023",
abstract = "The effects of glucocorticoid excess on regulation of insulin receptors were investigated in dexamethasone-treated rats. Glucocorticoid excess was produced by administration of dexamethasone (0.5 mg/100 g b.w.) 30 min, 4, 12, 18, 24, 42 or 70 h before experiments. This treatment caused time-dependent changes of glucose and insulin concentration in blood, as well as in amounts of specific insulin binding and insulin receptors of liver cells and erythrocytes. The time intervals in which dexamethasone produced the increase in insulin concentration were accompanied with decrease in insulin binding to receptors in membranes of liver cells, while significant changes in insulin binding to receptors of erythrocytes were not observed under the same experimental conditions. The effect is maximal 18 and 42 h after dexamethasone treatment that increase insulin blood level by about 85% and 60%, respectively. Receptor analysis revealed that changes in specific binding of insulin could be due to significant changes in amount of binding sites on cell surface rather than to mild alteration in receptor affinity. These findings suggest that besides the changes in insulin level, the alterations in insulin receptor number and affinity may play a major role in the states of altered insulin sensitivity which accompany glucocorticoid excess.",
journal = "General Physiology and Biophysics",
title = "Time dependent effects of dexamethasone on serum insulin level and insulin receptors in rat liver and erythrocytes",
volume = "25",
number = "1",
pages = "11-24"
}
Korićanac, G., Isenović, E. R., Stojanovic-Susulic, V., Miskovic, D., Žakula, Z.,& Ribarac-Stepić, N. B. (2006). Time dependent effects of dexamethasone on serum insulin level and insulin receptors in rat liver and erythrocytes.
General Physiology and Biophysics, 25(1), 11-24.
Korićanac G, Isenović ER, Stojanovic-Susulic V, Miskovic D, Žakula Z, Ribarac-Stepić NB. Time dependent effects of dexamethasone on serum insulin level and insulin receptors in rat liver and erythrocytes. General Physiology and Biophysics. 2006;25(1):11-24
Korićanac Goran, Isenović Esma R., Stojanovic-Susulic V, Miskovic D, Žakula Zorica, Ribarac-Stepić Nevena B., "Time dependent effects of dexamethasone on serum insulin level and insulin receptors in rat liver and erythrocytes" General Physiology and Biophysics, 25, no. 1 (2006):11-24
7

Molecular basis of glucocorticoid action

Ribarac-Stepić, Nevena B.; Đurica, Snežana N.; Žakula, Zorica; Korićanac, Goran; Milošević, Dragoslav P.

(2005)

TY  - JOUR
AU  - Ribarac-Stepić, Nevena B.
AU  - Đurica, Snežana N.
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Milošević, Dragoslav P.
PY  - 2005
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0370-817905061R
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7805
AB  - Glucocorticoid hormones are involved in regulation of cell processes and coordinate physiological response to diverse signals. These hormones, through interaction with specific intracellular receptors, coordinate components of physiological repertoires by activating the expression of gene networks. Thus hormone-receptor complexes may function as key constituent in regulation of specific cell functions as well as in provoking differentiation in already determined cells. Analysis of steroid receptors are important for understanding of molecular details of transcriptional control as well as providing the insight as to how an individual transcriptional factor such as glucocorticoid receptor, contributes to cell identity and function. The purpose of this review is to establish the general molecular mechanism of glucocorticoid action and mechanism associated hormone-receptor complexes with the control of differential patterns (i.e. "positive" and "negative") of gene expression. One of the examples of two signal pathways regulating opposite gene expression are NF-kB and GR-mediated signal pathways. These pathways have important and opposite roles in the immune function. NF-kB is transcription factor which induces the expression of many genes that participate in immune and inflamatory response, while GR is transcription factor that serves as antiinflammatory agent and immune suppressor. Their interactions within the cell, although not yet completely understood, appear to be an important, possibly even the primary mechanism of immune homeostasis. It has not been established that glucocorticoid sensitivity can be caused by mechanisms other than changes of GR number and properties, although recent studies have indicated that receptor isoforms and transcriptional factors may modulate glucocorticoid responsiveness by interacting with receptor protein or directly at the site of DNA binding. The aim of this review is also to describe the role of glucocorticoid receptors in mechanism of glucocorticoid action on cell functions, including immune responses, as well as to present emerging issues on clinical aspects of molecular mechanisms of glucocorticoid action.
T2  - Srpski arhiv za celokupno lekarstvo
T1  - Molecular basis of glucocorticoid action
T1  - Молекулска основа деловања гликокортикоида
VL  - 133
IS  - Suppl. 1
SP  - 61
EP  - 66
DO  - 10.2298/SARH05S1061R
ER  - 
@article{
author = "Ribarac-Stepić, Nevena B. and Đurica, Snežana N. and Žakula, Zorica and Korićanac, Goran and Milošević, Dragoslav P.",
year = "2005",
url = "http://www.doiserbia.nb.rs/Article.aspx?ID=0370-817905061R, http://vinar.vin.bg.ac.rs/handle/123456789/7805",
abstract = "Glucocorticoid hormones are involved in regulation of cell processes and coordinate physiological response to diverse signals. These hormones, through interaction with specific intracellular receptors, coordinate components of physiological repertoires by activating the expression of gene networks. Thus hormone-receptor complexes may function as key constituent in regulation of specific cell functions as well as in provoking differentiation in already determined cells. Analysis of steroid receptors are important for understanding of molecular details of transcriptional control as well as providing the insight as to how an individual transcriptional factor such as glucocorticoid receptor, contributes to cell identity and function. The purpose of this review is to establish the general molecular mechanism of glucocorticoid action and mechanism associated hormone-receptor complexes with the control of differential patterns (i.e. "positive" and "negative") of gene expression. One of the examples of two signal pathways regulating opposite gene expression are NF-kB and GR-mediated signal pathways. These pathways have important and opposite roles in the immune function. NF-kB is transcription factor which induces the expression of many genes that participate in immune and inflamatory response, while GR is transcription factor that serves as antiinflammatory agent and immune suppressor. Their interactions within the cell, although not yet completely understood, appear to be an important, possibly even the primary mechanism of immune homeostasis. It has not been established that glucocorticoid sensitivity can be caused by mechanisms other than changes of GR number and properties, although recent studies have indicated that receptor isoforms and transcriptional factors may modulate glucocorticoid responsiveness by interacting with receptor protein or directly at the site of DNA binding. The aim of this review is also to describe the role of glucocorticoid receptors in mechanism of glucocorticoid action on cell functions, including immune responses, as well as to present emerging issues on clinical aspects of molecular mechanisms of glucocorticoid action.",
journal = "Srpski arhiv za celokupno lekarstvo",
title = "Molecular basis of glucocorticoid action, Молекулска основа деловања гликокортикоида",
volume = "133",
number = "Suppl. 1",
pages = "61-66",
doi = "10.2298/SARH05S1061R"
}
Ribarac-Stepić, N. B., Đurica, S. N., Žakula, Z., Korićanac, G.,& Milošević, D. P. (2005). Молекулска основа деловања гликокортикоида.
Srpski arhiv za celokupno lekarstvo, 133(Suppl. 1), 61-66.
https://doi.org/10.2298/SARH05S1061R
Ribarac-Stepić NB, Đurica SN, Žakula Z, Korićanac G, Milošević DP. Молекулска основа деловања гликокортикоида. Srpski arhiv za celokupno lekarstvo. 2005;133(Suppl. 1):61-66
Ribarac-Stepić Nevena B., Đurica Snežana N., Žakula Zorica, Korićanac Goran, Milošević Dragoslav P., "Молекулска основа деловања гликокортикоида" Srpski arhiv za celokupno lekarstvo, 133, no. Suppl. 1 (2005):61-66,
https://doi.org/10.2298/SARH05S1061R .
1
1