TY  - JOUR
AU  - Prodanović, Radiša
AU  - Kirovski, Danijela
AU  - Vujanac, Ivan
AU  - Đorđević, Ana D.
AU  - Romić, Snježana Đ.
AU  - Pantelić, Marija
AU  - Korićanac, Goran
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10356
AB  - A number of alterations have been identified in lipid metabolism within adipose tissue and liver in obesity. Less is known about the capacity of skeletal muscle for the metabolism of fatty acids in obesity-related insulin resistance, though it is evident that dry cow muscles may contain increased triglyceride content. The current study was therefore undertaken to evaluate the skeletal muscle expression of proteins of the fatty acid metabolism in dry cows with different body condition scores (BCS). Sixteen Holstein-Friesian close-up cows were divided into 2 equal groups based on their BCS as optimal (3.25 ≤ BCS ≤ 3.5) and high (4.0 ≤ BCS ≤ 4.25). Blood samples collection and skeletal muscle biopsies were carried out at day 10 before calving. Blood serum was assayed for concentration of resistin using a bovine specific ELISA. Protein expression of insulin receptor beta subunit (IRβ), glucose transporter 4 (GLUT4), fatty acid translocase (FAT/CD36), fatty acid transporter 1 (FATP1), carnitine palmitoyltransferase 1 (CPT1), AMP-acitvated protein kinase (AMPK) and lipin 1 were analyzed in semitendinosus muscle by immunoblot. Resistin differed non-significantly between high-BCS and optimal-BCS cows. Insulin-resistant lipid metabolism in obese cows was paralleled with increased skeletal muscle expression of lipin 1 and GLUT4, and decreased expression of IRβ and FATP1. These data suggest that in obesity-related insulin resistance, metabolic capacity in dry cow skeletal muscles appears to be organized towards the synthesis of signaling intermediates rather than fatty acids oxidation and that altered fatty acid uptake does not contribute to this disposition.
T2  - Research in Veterinary Science
T1  - Obesity-related prepartal insulin resistance in dairy cows is associated with increased lipin 1 and decreased FATP 1 expression in skeletal muscle
VL  - 150
SP  - 189
EP  - 194
DO  - 10.1016/j.rvsc.2022.04.012
ER  - 

@article{
author = "Prodanović, Radiša and Kirovski, Danijela and Vujanac, Ivan and Đorđević, Ana D. and Romić, Snježana Đ. and Pantelić, Marija and Korićanac, Goran",
year = "2022",
abstract = "A number of alterations have been identified in lipid metabolism within adipose tissue and liver in obesity. Less is known about the capacity of skeletal muscle for the metabolism of fatty acids in obesity-related insulin resistance, though it is evident that dry cow muscles may contain increased triglyceride content. The current study was therefore undertaken to evaluate the skeletal muscle expression of proteins of the fatty acid metabolism in dry cows with different body condition scores (BCS). Sixteen Holstein-Friesian close-up cows were divided into 2 equal groups based on their BCS as optimal (3.25 ≤ BCS ≤ 3.5) and high (4.0 ≤ BCS ≤ 4.25). Blood samples collection and skeletal muscle biopsies were carried out at day 10 before calving. Blood serum was assayed for concentration of resistin using a bovine specific ELISA. Protein expression of insulin receptor beta subunit (IRβ), glucose transporter 4 (GLUT4), fatty acid translocase (FAT/CD36), fatty acid transporter 1 (FATP1), carnitine palmitoyltransferase 1 (CPT1), AMP-acitvated protein kinase (AMPK) and lipin 1 were analyzed in semitendinosus muscle by immunoblot. Resistin differed non-significantly between high-BCS and optimal-BCS cows. Insulin-resistant lipid metabolism in obese cows was paralleled with increased skeletal muscle expression of lipin 1 and GLUT4, and decreased expression of IRβ and FATP1. These data suggest that in obesity-related insulin resistance, metabolic capacity in dry cow skeletal muscles appears to be organized towards the synthesis of signaling intermediates rather than fatty acids oxidation and that altered fatty acid uptake does not contribute to this disposition.",
journal = "Research in Veterinary Science",
title = "Obesity-related prepartal insulin resistance in dairy cows is associated with increased lipin 1 and decreased FATP 1 expression in skeletal muscle",
volume = "150",
pages = "189-194",
doi = "10.1016/j.rvsc.2022.04.012"
}

Prodanović, R., Kirovski, D., Vujanac, I., Đorđević, A. D., Romić, S. Đ., Pantelić, M.,& Korićanac, G.. (2022). Obesity-related prepartal insulin resistance in dairy cows is associated with increased lipin 1 and decreased FATP 1 expression in skeletal muscle. in Research in Veterinary Science, 150, 189-194.
https://doi.org/10.1016/j.rvsc.2022.04.012

Prodanović R, Kirovski D, Vujanac I, Đorđević AD, Romić SĐ, Pantelić M, Korićanac G. Obesity-related prepartal insulin resistance in dairy cows is associated with increased lipin 1 and decreased FATP 1 expression in skeletal muscle. in Research in Veterinary Science. 2022;150:189-194.
doi:10.1016/j.rvsc.2022.04.012 .

Prodanović, Radiša, Kirovski, Danijela, Vujanac, Ivan, Đorđević, Ana D., Romić, Snježana Đ., Pantelić, Marija, Korićanac, Goran, "Obesity-related prepartal insulin resistance in dairy cows is associated with increased lipin 1 and decreased FATP 1 expression in skeletal muscle" in Research in Veterinary Science, 150 (2022):189-194,
https://doi.org/10.1016/j.rvsc.2022.04.012 . .

TY  - JOUR
AU  - Bundalo, Maja M.
AU  - Đorđević, Ana D.
AU  - Bursać, Biljana
AU  - Živković, Maja
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1839
AB  - The adipose tissue renin-angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.
T2  - Applied Physiology Nutrition and Metabolism
T1  - Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue
VL  - 42
IS  - 12
SP  - 1254
EP  - 1263
DO  - 10.1139/apnm-2016-0725
ER  - 

@article{
author = "Bundalo, Maja M. and Đorđević, Ana D. and Bursać, Biljana and Živković, Maja and Korićanac, Goran and Stanković, Aleksandra",
year = "2017",
abstract = "The adipose tissue renin-angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.",
journal = "Applied Physiology Nutrition and Metabolism",
title = "Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue",
volume = "42",
number = "12",
pages = "1254-1263",
doi = "10.1139/apnm-2016-0725"
}

Bundalo, M. M., Đorđević, A. D., Bursać, B., Živković, M., Korićanac, G.,& Stanković, A.. (2017). Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue. in Applied Physiology Nutrition and Metabolism, 42(12), 1254-1263.
https://doi.org/10.1139/apnm-2016-0725

Bundalo MM, Đorđević AD, Bursać B, Živković M, Korićanac G, Stanković A. Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue. in Applied Physiology Nutrition and Metabolism. 2017;42(12):1254-1263.
doi:10.1139/apnm-2016-0725 .

Bundalo, Maja M., Đorđević, Ana D., Bursać, Biljana, Živković, Maja, Korićanac, Goran, Stanković, Aleksandra, "Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue" in Applied Physiology Nutrition and Metabolism, 42, no. 12 (2017):1254-1263,
https://doi.org/10.1139/apnm-2016-0725 . .

TY  - JOUR
AU  - Prodanović, Radiša
AU  - Korićanac, Goran
AU  - Vujanac, Ivan
AU  - Đorđević, Ana D.
AU  - Pantelić, Marija
AU  - Romić, Snježana Đ.
AU  - Stanimirovic, Zoran
AU  - Kirovski, Danijela
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1211
AB  - We investigated the hypothesis that obesity in dairy cows enhanced expression of proteins involved in hepatic fatty acid uptake and metabolism. Sixteen Holstein-Friesian close-up cows were divided into 2 equal groups based on their body condition score (BCS) as optimal (3.25 LT = BCS LT = 3.5) and high (4.0 LT = BCS LT = 425). Intravenous glucose tolerance test (GTT) and liver biopsies were carried out at day 10 before calving. Blood samples were collected before (basal) and after glucose infusion, and glucose, insulin and non-esterified fatty acid (NEFA) levels were determined at each sample point. In addition, beta-hydroxybutyrate and triglycerides levels were measured in the basal samples. The liver biopsies were analyzed for total lipid content and protein expression of insulin receptor beta (IR beta), fatty acid translocase (FAT/CD36) and sterol regulatory element-binding protein-1 (SREBP-1). Basal glucose and insulin were higher in high-BCS cows, which coincided with higher circulating triglycerides and hepatic lipid content. Clearance rate and AUC for NEFA during GTT were higher in optimal-BCS cows. The development of insulin resistance and fatty liver in obese cows was paralleled by increased hepatic expression of the IR beta, CD36 and SREBP-1. These results suggest that increased expression of hepatic CD36 and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation. (C) 2016 Elsevier Ltd. All rights reserved.
T2  - Research in Veterinary Science
T1  - Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression
VL  - 107
SP  - 16
EP  - 19
DO  - 10.1016/j.rvsc.2016.04.007
ER  - 

@article{
author = "Prodanović, Radiša and Korićanac, Goran and Vujanac, Ivan and Đorđević, Ana D. and Pantelić, Marija and Romić, Snježana Đ. and Stanimirovic, Zoran and Kirovski, Danijela",
year = "2016",
abstract = "We investigated the hypothesis that obesity in dairy cows enhanced expression of proteins involved in hepatic fatty acid uptake and metabolism. Sixteen Holstein-Friesian close-up cows were divided into 2 equal groups based on their body condition score (BCS) as optimal (3.25 LT = BCS LT = 3.5) and high (4.0 LT = BCS LT = 425). Intravenous glucose tolerance test (GTT) and liver biopsies were carried out at day 10 before calving. Blood samples were collected before (basal) and after glucose infusion, and glucose, insulin and non-esterified fatty acid (NEFA) levels were determined at each sample point. In addition, beta-hydroxybutyrate and triglycerides levels were measured in the basal samples. The liver biopsies were analyzed for total lipid content and protein expression of insulin receptor beta (IR beta), fatty acid translocase (FAT/CD36) and sterol regulatory element-binding protein-1 (SREBP-1). Basal glucose and insulin were higher in high-BCS cows, which coincided with higher circulating triglycerides and hepatic lipid content. Clearance rate and AUC for NEFA during GTT were higher in optimal-BCS cows. The development of insulin resistance and fatty liver in obese cows was paralleled by increased hepatic expression of the IR beta, CD36 and SREBP-1. These results suggest that increased expression of hepatic CD36 and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation. (C) 2016 Elsevier Ltd. All rights reserved.",
journal = "Research in Veterinary Science",
title = "Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression",
volume = "107",
pages = "16-19",
doi = "10.1016/j.rvsc.2016.04.007"
}

Prodanović, R., Korićanac, G., Vujanac, I., Đorđević, A. D., Pantelić, M., Romić, S. Đ., Stanimirovic, Z.,& Kirovski, D.. (2016). Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression. in Research in Veterinary Science, 107, 16-19.
https://doi.org/10.1016/j.rvsc.2016.04.007

Prodanović R, Korićanac G, Vujanac I, Đorđević AD, Pantelić M, Romić SĐ, Stanimirovic Z, Kirovski D. Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression. in Research in Veterinary Science. 2016;107:16-19.
doi:10.1016/j.rvsc.2016.04.007 .

Prodanović, Radiša, Korićanac, Goran, Vujanac, Ivan, Đorđević, Ana D., Pantelić, Marija, Romić, Snježana Đ., Stanimirovic, Zoran, Kirovski, Danijela, "Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression" in Research in Veterinary Science, 107 (2016):16-19,
https://doi.org/10.1016/j.rvsc.2016.04.007 . .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Mitić, Miloš
AU  - Lukić, Iva
AU  - Radojčić, Marija B.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/270
AB  - Knowledge of the antioxidant defense in the stress-responding structures of the CNS is of crucial importance, since oxidative damage is a phenomenon accompanying many stress-related disorders. Regulation of antioxidative and anti-inflammatory defense through Nrf2 (nuclear factor 2 eritroid related factor 2) pathway has emerged as a promising approach for neuroprotection. In this study, we used chronic social isolation of male Wistar rats to induce depressive-like behavior. We hypothesized that Nrf2 Keap1 pathway is compromised in the limbic brain after prolonged stress. Since subcellular trafficking of Nrf2 and its inhibitor Keap1 (Kelch ECH associating protein 1) is essential for the activation of Nrf2, we determined their protein level in cytosolic and nuclear comp and linents of hippocampus and prefrontal cortex (PEG). We also determined mRNA levels of Nr12-regulated genes involved in the production and utilization of glutathione, glutamate cysteine ligase (Gclm), glutathione S-transferase (Gsta3) and glutathione reductase (Gsr). Our results showed that chronic isolation induced anxiety and depressive-like behavior, decreased Nrf2 and in parallel increased Keap1 and nuclear factor kappa B (NF kappa B) in the hippocampus, which were not accompanied by expression profiles of Nrf2-regulated genes. Chronically stressed rats challenged with acute stress failed to induce any response of examined genes in either of brain structures, even though Nrf2/Keap1 was altered, while in naive animals Nrf2 activity corresponded witli an expression of Nrf2-regulated genes. Our results reveal maladaptive character of chronic stress at Nrf2/Keap1 level followed by pro-inflammatory conditions, and suggest a possible role of these alterations in pathogenesis of depressive/anxiety disorders. (C) 2015 Elsevier B.V. All rights reserved.
T2  - Brain Research
T1  - Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress
VL  - 1602
SP  - 20
EP  - 31
DO  - 10.1016/j.brainres.2015.01.010
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Mitić, Miloš and Lukić, Iva and Radojčić, Marija B.",
year = "2015",
abstract = "Knowledge of the antioxidant defense in the stress-responding structures of the CNS is of crucial importance, since oxidative damage is a phenomenon accompanying many stress-related disorders. Regulation of antioxidative and anti-inflammatory defense through Nrf2 (nuclear factor 2 eritroid related factor 2) pathway has emerged as a promising approach for neuroprotection. In this study, we used chronic social isolation of male Wistar rats to induce depressive-like behavior. We hypothesized that Nrf2 Keap1 pathway is compromised in the limbic brain after prolonged stress. Since subcellular trafficking of Nrf2 and its inhibitor Keap1 (Kelch ECH associating protein 1) is essential for the activation of Nrf2, we determined their protein level in cytosolic and nuclear comp and linents of hippocampus and prefrontal cortex (PEG). We also determined mRNA levels of Nr12-regulated genes involved in the production and utilization of glutathione, glutamate cysteine ligase (Gclm), glutathione S-transferase (Gsta3) and glutathione reductase (Gsr). Our results showed that chronic isolation induced anxiety and depressive-like behavior, decreased Nrf2 and in parallel increased Keap1 and nuclear factor kappa B (NF kappa B) in the hippocampus, which were not accompanied by expression profiles of Nrf2-regulated genes. Chronically stressed rats challenged with acute stress failed to induce any response of examined genes in either of brain structures, even though Nrf2/Keap1 was altered, while in naive animals Nrf2 activity corresponded witli an expression of Nrf2-regulated genes. Our results reveal maladaptive character of chronic stress at Nrf2/Keap1 level followed by pro-inflammatory conditions, and suggest a possible role of these alterations in pathogenesis of depressive/anxiety disorders. (C) 2015 Elsevier B.V. All rights reserved.",
journal = "Brain Research",
title = "Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress",
volume = "1602",
pages = "20-31",
doi = "10.1016/j.brainres.2015.01.010"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M., Mitić, M., Lukić, I.,& Radojčić, M. B.. (2015). Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress. in Brain Research, 1602, 20-31.
https://doi.org/10.1016/j.brainres.2015.01.010

Đorđević JD, Đorđević AD, Adžić M, Mitić M, Lukić I, Radojčić MB. Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress. in Brain Research. 2015;1602:20-31.
doi:10.1016/j.brainres.2015.01.010 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Mitić, Miloš, Lukić, Iva, Radojčić, Marija B., "Alterations in the Nrf2-Keap1 signaling pathway and its downstream target genes in rat brain under stress" in Brain Research, 1602 (2015):20-31,
https://doi.org/10.1016/j.brainres.2015.01.010 . .

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Tepavčević, Snežana
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Radoičić, Marija B.
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/93
AB  - Introduction: We investigated the effects of ghrelin on protein expression of the liver antioxidant enzymes superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), nuclear factor kappa B (NF kappa B) and inducible nitric oxide synthase (iNOS). Furthermore, we aimed to investigate whether extracellular regulated protein kinase (ERK1/2) and protein kinase B (Akt) are involved in ghrelin-regulated liver antioxidant enzymes and iNOS protein expression. Material and methods: Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) injected into the lateral cerebral ventricle every 24 h for 5 days, and 2 h after the last treatment the animals were sacrificed and the liver excised. The Western blot method was used to determine expression of antioxidant enzymes, iNOS, phosphorylation of Akt, ERK1/2 and nuclear factor kappa B (NF kappa B) subunits 50 and 65. Results: There was significantly higher protein expression of CuZnSOD (p LT 0.001), MnSOD (p LT 0.001), CAT (p LT 0.001), GPx, (p LT 0.001), and GR (p LT 0.01) in the liver isolated from ghrelin-treated animals compared with control animals. In contrast, ghrelin significantly (p LT 0.01) reduced protein expression of iNOS. In addition, phosphorylation of NF kappa B subunits p65 and p50 was significantly (p LT 0.001 for p65; p LT 0.05 for p50) reduced by ghrelin when compared with controls. Phosphorylation of ERK1/2 and of Akt was significantly higher in ghrelin-treated than in control animals (p LT 0.05 for ERK1/2; p LT 0.01 for Akt). Conclusions: The results show that activation of Akt and ERK1/2 is involved in ghrelin-mediated regulation of protein expression of antioxidant enzymes and iNOS in the rat liver.
T2  - Archives of Medical Science
T1  - Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver
VL  - 10
IS  - 4
SP  - 806
EP  - 816
DO  - 10.5114/aoms.2014.44872
ER  - 

@article{
author = "Dobutović, Branislava and Sudar, Emina and Tepavčević, Snežana and Đorđević, Jelena D. and Đorđević, Ana D. and Radoičić, Marija B. and Isenović, Esma R.",
year = "2014",
abstract = "Introduction: We investigated the effects of ghrelin on protein expression of the liver antioxidant enzymes superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), nuclear factor kappa B (NF kappa B) and inducible nitric oxide synthase (iNOS). Furthermore, we aimed to investigate whether extracellular regulated protein kinase (ERK1/2) and protein kinase B (Akt) are involved in ghrelin-regulated liver antioxidant enzymes and iNOS protein expression. Material and methods: Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) injected into the lateral cerebral ventricle every 24 h for 5 days, and 2 h after the last treatment the animals were sacrificed and the liver excised. The Western blot method was used to determine expression of antioxidant enzymes, iNOS, phosphorylation of Akt, ERK1/2 and nuclear factor kappa B (NF kappa B) subunits 50 and 65. Results: There was significantly higher protein expression of CuZnSOD (p LT 0.001), MnSOD (p LT 0.001), CAT (p LT 0.001), GPx, (p LT 0.001), and GR (p LT 0.01) in the liver isolated from ghrelin-treated animals compared with control animals. In contrast, ghrelin significantly (p LT 0.01) reduced protein expression of iNOS. In addition, phosphorylation of NF kappa B subunits p65 and p50 was significantly (p LT 0.001 for p65; p LT 0.05 for p50) reduced by ghrelin when compared with controls. Phosphorylation of ERK1/2 and of Akt was significantly higher in ghrelin-treated than in control animals (p LT 0.05 for ERK1/2; p LT 0.01 for Akt). Conclusions: The results show that activation of Akt and ERK1/2 is involved in ghrelin-mediated regulation of protein expression of antioxidant enzymes and iNOS in the rat liver.",
journal = "Archives of Medical Science",
title = "Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver",
volume = "10",
number = "4",
pages = "806-816",
doi = "10.5114/aoms.2014.44872"
}

Dobutović, B., Sudar, E., Tepavčević, S., Đorđević, J. D., Đorđević, A. D., Radoičić, M. B.,& Isenović, E. R.. (2014). Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver. in Archives of Medical Science, 10(4), 806-816.
https://doi.org/10.5114/aoms.2014.44872

Dobutović B, Sudar E, Tepavčević S, Đorđević JD, Đorđević AD, Radoičić MB, Isenović ER. Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver. in Archives of Medical Science. 2014;10(4):806-816.
doi:10.5114/aoms.2014.44872 .

Dobutović, Branislava, Sudar, Emina, Tepavčević, Snežana, Đorđević, Jelena D., Đorđević, Ana D., Radoičić, Marija B., Isenović, Esma R., "Effects of ghrelin on protein expression of antioxidative enzymes and iNOS in the rat liver" in Archives of Medical Science, 10, no. 4 (2014):806-816,
https://doi.org/10.5114/aoms.2014.44872 . .

TY  - JOUR
AU  - Velickovic, Natasa A.
AU  - Đorđević, Ana D.
AU  - Drakulić, Dunja R.
AU  - Šećerov, Bojana Lj.
AU  - Grković, Ivana
AU  - Milošević, Maja
AU  - Horvat, Anica
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5594
AB  - Ionizing radiation is commonly used in the treatment of brain tumors but it can impair cognitive functions, such as learning and memory. Since cognitive dysfunctions are predominantly result of cell death by apoptosis in hippocampal cells, in this study we analyzed acute effects of cranial gamma-irradiation (10 Gy) on-expression-of proapoptotic molecules (p53, Box) and antiapoptotic molecule Bcl-2, as well as caspase-3 activation and cytochrome c redistribution in the hippocampus of young rats. The selected regimen of irradiation resembles the established animal model for childhood prophylactic cranial radiotherapy. Our results demonstrated that p53 mRNA expression was unchanged after irradiation, while induction of p53 protein was rapid. In parallel, Bax mRNA and protein levels were also increased following irradiation, whereas Bcl-2 expression was not changed during the examined post-irradiation period. These changes were accompanied with early hallmarks of apoptosis, such as increased cytochrome c release and stimulated activation of caspase-3. Overall, this study demonstrates that cranial irradiation is associated with the augmented apoptotic pathway in the rat hippocampus, which could be related to the cognitive decline observed in patients after prophylactic cranial radiotherapy, but also opens perspective in finding radioprotectors that can mitigate radiation injury of normal brain tissue.
T2  - Nuclear technology and radiation protection
T1  - Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus
VL  - 28
IS  - 2
SP  - 212
EP  - 220
DO  - 10.2298/NTRP1302212V
ER  - 

@article{
author = "Velickovic, Natasa A. and Đorđević, Ana D. and Drakulić, Dunja R. and Šećerov, Bojana Lj. and Grković, Ivana and Milošević, Maja and Horvat, Anica",
year = "2013",
abstract = "Ionizing radiation is commonly used in the treatment of brain tumors but it can impair cognitive functions, such as learning and memory. Since cognitive dysfunctions are predominantly result of cell death by apoptosis in hippocampal cells, in this study we analyzed acute effects of cranial gamma-irradiation (10 Gy) on-expression-of proapoptotic molecules (p53, Box) and antiapoptotic molecule Bcl-2, as well as caspase-3 activation and cytochrome c redistribution in the hippocampus of young rats. The selected regimen of irradiation resembles the established animal model for childhood prophylactic cranial radiotherapy. Our results demonstrated that p53 mRNA expression was unchanged after irradiation, while induction of p53 protein was rapid. In parallel, Bax mRNA and protein levels were also increased following irradiation, whereas Bcl-2 expression was not changed during the examined post-irradiation period. These changes were accompanied with early hallmarks of apoptosis, such as increased cytochrome c release and stimulated activation of caspase-3. Overall, this study demonstrates that cranial irradiation is associated with the augmented apoptotic pathway in the rat hippocampus, which could be related to the cognitive decline observed in patients after prophylactic cranial radiotherapy, but also opens perspective in finding radioprotectors that can mitigate radiation injury of normal brain tissue.",
journal = "Nuclear technology and radiation protection",
title = "Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus",
volume = "28",
number = "2",
pages = "212-220",
doi = "10.2298/NTRP1302212V"
}

Velickovic, N. A., Đorđević, A. D., Drakulić, D. R., Šećerov, B. Lj., Grković, I., Milošević, M.,& Horvat, A.. (2013). Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus. in Nuclear technology and radiation protection, 28(2), 212-220.
https://doi.org/10.2298/NTRP1302212V

Velickovic NA, Đorđević AD, Drakulić DR, Šećerov BL, Grković I, Milošević M, Horvat A. Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus. in Nuclear technology and radiation protection. 2013;28(2):212-220.
doi:10.2298/NTRP1302212V .

Velickovic, Natasa A., Đorđević, Ana D., Drakulić, Dunja R., Šećerov, Bojana Lj., Grković, Ivana, Milošević, Maja, Horvat, Anica, "Radiation-Mediated Induction of Apoptotic Cell Death in Rat Hippocampus" in Nuclear technology and radiation protection, 28, no. 2 (2013):212-220,
https://doi.org/10.2298/NTRP1302212V . .

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  - https://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",
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. in 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. in Archives of Biological Sciences. 2013;65(2):455-464.
doi:10.2298/ABS1302455K .

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" in Archives of Biological Sciences, 65, no. 2 (2013):455-464,
https://doi.org/10.2298/ABS1302455K . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Lukić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Đorđević, Ana D.
AU  - Krstić-Demonacos, Marija
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5868
AB  - Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism
VL  - 38
IS  - 12
SP  - 2914
EP  - 2924
DO  - 10.1016/j.psyneuen.2013.07.019
ER  - 

@article{
author = "Adžić, Miroslav and Lukić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Elaković, Ivana and Đorđević, Ana D. and Krstić-Demonacos, Marija and Matić, Gordana and Radojčić, Marija",
year = "2013",
abstract = "Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism",
volume = "38",
number = "12",
pages = "2914-2924",
doi = "10.1016/j.psyneuen.2013.07.019"
}

Adžić, M., Lukić, I., Mitić, M., Đorđević, J. D., Elaković, I., Đorđević, A. D., Krstić-Demonacos, M., Matić, G.,& Radojčić, M.. (2013). Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology, 38(12), 2914-2924.
https://doi.org/10.1016/j.psyneuen.2013.07.019

Adžić M, Lukić I, Mitić M, Đorđević JD, Elaković I, Đorđević AD, Krstić-Demonacos M, Matić G, Radojčić M. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology. 2013;38(12):2914-2924.
doi:10.1016/j.psyneuen.2013.07.019 .

Adžić, Miroslav, Lukić, Iva, Mitić, Miloš, Đorđević, Jelena D., Elaković, Ivana, Đorđević, Ana D., Krstić-Demonacos, Marija, Matić, Gordana, Radojčić, Marija, "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism" in Psychoneuroendocrinology, 38, no. 12 (2013):2914-2924,
https://doi.org/10.1016/j.psyneuen.2013.07.019 . .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4678
AB  - Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-psychopharmacology and Biological Psychiatry
T1  - Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats
VL  - 36
IS  - 1
SP  - 92
EP  - 100
DO  - 10.1016/j.pnpbp.2011.10.006
ER  - 

@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radoičić, Marija B.",
year = "2012",
abstract = "Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-psychopharmacology and Biological Psychiatry",
title = "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats",
volume = "36",
number = "1",
pages = "92-100",
doi = "10.1016/j.pnpbp.2011.10.006"
}

Đorđević, A. D., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radoičić, M. B.. (2012). Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. in Progress in Neuro-psychopharmacology and Biological Psychiatry, 36(1), 92-100.
https://doi.org/10.1016/j.pnpbp.2011.10.006

Đorđević AD, Đorđević JD, Elaković I, Adžić M, Matić G, Radoičić MB. Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. in Progress in Neuro-psychopharmacology and Biological Psychiatry. 2012;36(1):92-100.
doi:10.1016/j.pnpbp.2011.10.006 .

Đorđević, Ana D., Đorđević, Jelena D., Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radoičić, Marija B., "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats" in Progress in Neuro-psychopharmacology and Biological Psychiatry, 36, no. 1 (2012):92-100,
https://doi.org/10.1016/j.pnpbp.2011.10.006 . .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4995
AB  - Chronic stress is a contributing risk factor in the development of psychiatric illnesses, including depressive disorders. The mechanisms of their psychopathology are multifaceted and include, besides others, alterations in the brain plasticity. Previously, we investigated the effects of chronic social stress in the limbic brain structures of Wistar rats (hippocampus, HIPPO, and prefrontal cortex, PFC) and found multiple characteristics that resembled alterations described in some clinical studies of depression. We extended our investigations and followed the behavior of stressed animals by the open field test (OFT) and forced swimming test (FST), and the expression and polysialylation of synaptic plasticity markers, neural cell adhesion molecule (NCAM) and L1, in the HIPPO and PFC. We also determined the adrenal gland mass and plasma corticosterone (CORT) as a terminal part of the hypothalamic-pituitary-adrenal axis activity. Our data indicated that stressed animals avoided the central zone in the OFT and displayed decreased swimming, but prolonged immobility in the FST. The animals exhibited marked hypertrophy of the adrenal gland cortex, in spite of decreased serum CORT. Simultaneously, the stressed animals exhibited an increase in NCAM mRNA expression in the HIPPO, but not in the PFC. The synaptosomal NCAM of the HIPPO was markedly polysialylated, while cortical PSA-NCAM was significantly decreased. The results showed that chronic social isolation of Wistar rats causes both anxiety-like and depression-like behavior. These alterations are parallel with molecular changes in the limbic brain, including diminished NCAM sialylation in the PFC. Together with our previous results, the current observations suggest that a chronic social isolation model may potentially be used to study molecular mechanisms that underlie depressive symptomatology. Copyright (c) 2012 S. Karger AG, Basel
T2  - Neuropsychobiology
T1  - Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers
VL  - 66
IS  - 2
SP  - 112
EP  - 119
DO  - 10.1159/000338605
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Radojčić, Marija",
year = "2012",
abstract = "Chronic stress is a contributing risk factor in the development of psychiatric illnesses, including depressive disorders. The mechanisms of their psychopathology are multifaceted and include, besides others, alterations in the brain plasticity. Previously, we investigated the effects of chronic social stress in the limbic brain structures of Wistar rats (hippocampus, HIPPO, and prefrontal cortex, PFC) and found multiple characteristics that resembled alterations described in some clinical studies of depression. We extended our investigations and followed the behavior of stressed animals by the open field test (OFT) and forced swimming test (FST), and the expression and polysialylation of synaptic plasticity markers, neural cell adhesion molecule (NCAM) and L1, in the HIPPO and PFC. We also determined the adrenal gland mass and plasma corticosterone (CORT) as a terminal part of the hypothalamic-pituitary-adrenal axis activity. Our data indicated that stressed animals avoided the central zone in the OFT and displayed decreased swimming, but prolonged immobility in the FST. The animals exhibited marked hypertrophy of the adrenal gland cortex, in spite of decreased serum CORT. Simultaneously, the stressed animals exhibited an increase in NCAM mRNA expression in the HIPPO, but not in the PFC. The synaptosomal NCAM of the HIPPO was markedly polysialylated, while cortical PSA-NCAM was significantly decreased. The results showed that chronic social isolation of Wistar rats causes both anxiety-like and depression-like behavior. These alterations are parallel with molecular changes in the limbic brain, including diminished NCAM sialylation in the PFC. Together with our previous results, the current observations suggest that a chronic social isolation model may potentially be used to study molecular mechanisms that underlie depressive symptomatology. Copyright (c) 2012 S. Karger AG, Basel",
journal = "Neuropsychobiology",
title = "Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers",
volume = "66",
number = "2",
pages = "112-119",
doi = "10.1159/000338605"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M.,& Radojčić, M.. (2012). Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers. in Neuropsychobiology, 66(2), 112-119.
https://doi.org/10.1159/000338605

Đorđević JD, Đorđević AD, Adžić M, Radojčić M. Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers. in Neuropsychobiology. 2012;66(2):112-119.
doi:10.1159/000338605 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Radojčić, Marija, "Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers" in Neuropsychobiology, 66, no. 2 (2012):112-119,
https://doi.org/10.1159/000338605 . .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5042
AB  - The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex
VL  - 693
IS  - 1-3
SP  - 37
EP  - 44
DO  - 10.1016/j.ejphar.2012.07.042
ER  - 

@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radojčić, Marija",
year = "2012",
abstract = "The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex",
volume = "693",
number = "1-3",
pages = "37-44",
doi = "10.1016/j.ejphar.2012.07.042"
}

Đorđević, A. D., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radojčić, M.. (2012). Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology, 693(1-3), 37-44.
https://doi.org/10.1016/j.ejphar.2012.07.042

Đorđević AD, Đorđević JD, Elaković I, Adžić M, Matić G, Radojčić M. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology. 2012;693(1-3):37-44.
doi:10.1016/j.ejphar.2012.07.042 .

Đorđević, Ana D., Đorđević, Jelena D., Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radojčić, Marija, "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex" in European Journal of Pharmacology, 693, no. 1-3 (2012):37-44,
https://doi.org/10.1016/j.ejphar.2012.07.042 . .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4329
AB  - Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver
VL  - 659
IS  - 1
SP  - 61
EP  - 66
DO  - 10.1016/j.ejphar.2011.03.003
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Elaković, Ivana and Matić, Gordana and Radojčić, Marija",
year = "2011",
abstract = "Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver",
volume = "659",
number = "1",
pages = "61-66",
doi = "10.1016/j.ejphar.2011.03.003"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M., Elaković, I., Matić, G.,& Radojčić, M.. (2011). Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. in European Journal of Pharmacology, 659(1), 61-66.
https://doi.org/10.1016/j.ejphar.2011.03.003

Đorđević JD, Đorđević AD, Adžić M, Elaković I, Matić G, Radojčić M. Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. in European Journal of Pharmacology. 2011;659(1):61-66.
doi:10.1016/j.ejphar.2011.03.003 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Elaković, Ivana, Matić, Gordana, Radojčić, Marija, "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver" in European Journal of Pharmacology, 659, no. 1 (2011):61-66,
https://doi.org/10.1016/j.ejphar.2011.03.003 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Rackov, Gorjana
AU  - Đorđević, Ana D.
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4640
AB  - Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.
T2  - Acta Chimica Slovenica
T1  - Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats
VL  - 58
IS  - 4
SP  - 785
EP  - 791
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4640
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Mitić, Miloš and Simić, Iva and Rackov, Gorjana and Đorđević, Ana D. and Elaković, Ivana and Matić, Gordana and Radojčić, Marija",
year = "2011",
abstract = "Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.",
journal = "Acta Chimica Slovenica",
title = "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats",
volume = "58",
number = "4",
pages = "785-791",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4640"
}

Adžić, M., Đorđević, J. D., Mitić, M., Simić, I., Rackov, G., Đorđević, A. D., Elaković, I., Matić, G.,& Radojčić, M.. (2011). Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. in Acta Chimica Slovenica, 58(4), 785-791.
https://hdl.handle.net/21.15107/rcub_vinar_4640

Adžić M, Đorđević JD, Mitić M, Simić I, Rackov G, Đorđević AD, Elaković I, Matić G, Radojčić M. Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. in Acta Chimica Slovenica. 2011;58(4):785-791.
https://hdl.handle.net/21.15107/rcub_vinar_4640 .

Adžić, Miroslav, Đorđević, Jelena D., Mitić, Miloš, Simić, Iva, Rackov, Gorjana, Đorđević, Ana D., Elaković, Ivana, Matić, Gordana, Radojčić, Marija, "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats" in Acta Chimica Slovenica, 58, no. 4 (2011):785-791,
https://hdl.handle.net/21.15107/rcub_vinar_4640 .

TY  - JOUR
AU  - Elaković, Ivana
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
AU  - Matić, Gordana
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4277
AB  - Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.
T2  - Brain Research
T1  - Gender-specific response of brain corticosteroid receptors to stress and fluoxetine
VL  - 1384
SP  - 61
EP  - 68
DO  - 10.1016/j.brainres.2011.01.078
ER  - 

@article{
author = "Elaković, Ivana and Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radojčić, Marija and Matić, Gordana",
year = "2011",
abstract = "Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "Brain Research",
title = "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine",
volume = "1384",
pages = "61-68",
doi = "10.1016/j.brainres.2011.01.078"
}

Elaković, I., Đorđević, A. D., Adžić, M., Đorđević, J. D., Radojčić, M.,& Matić, G.. (2011). Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. in Brain Research, 1384, 61-68.
https://doi.org/10.1016/j.brainres.2011.01.078

Elaković I, Đorđević AD, Adžić M, Đorđević JD, Radojčić M, Matić G. Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. in Brain Research. 2011;1384:61-68.
doi:10.1016/j.brainres.2011.01.078 .

Elaković, Ivana, Đorđević, Ana D., Adžić, Miroslav, Đorđević, Jelena D., Radojčić, Marija, Matić, Gordana, "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine" in Brain Research, 1384 (2011):61-68,
https://doi.org/10.1016/j.brainres.2011.01.078 . .

TY  - CONF
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena
AU  - Elaković, Ivana
AU  - Simić, Iva
AU  - Mitić, Miloš
AU  - Rackov, Gorjana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9306
AB  - Alterations in the antioxidative defense parameters upon chronic stress are considered
critical for pathophysiology of stress related psychiatric disorders and their status in
blood serves as biomarker for effects of pharmacological treatments. We investigated
the modulation of erythrocyte antioxidant enzymes (AOEs): superoxide dismutase
(SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR)
protein expression and activity in Wistar male rats subjected to chronic psychosocial
isolation and/or treated with fluoxetine. Chronically isolated animals exhibited
decreased levels of plasma corticoserone (CORT). AOEs status was not altered either
by chronic social isolation or by fluoxetine. The only exception was GLR, whose level
and activity were both markedly reduced by fluoxetine. Our study indicates that
fluoxetine treatment of chronically isolated male Wistar rats, leads to significant
reduction in the level and activity of GLR in the erythrocytes.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
T1  - Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9306
ER  - 

@conference{
author = "Adžić, Miroslav and Đorđević, Ana D. and Đorđević, Jelena and Elaković, Ivana and Simić, Iva and Mitić, Miloš and Rackov, Gorjana and Matić, Gordana and Radojčić, Marija",
year = "2010",
abstract = "Alterations in the antioxidative defense parameters upon chronic stress are considered
critical for pathophysiology of stress related psychiatric disorders and their status in
blood serves as biomarker for effects of pharmacological treatments. We investigated
the modulation of erythrocyte antioxidant enzymes (AOEs): superoxide dismutase
(SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR)
protein expression and activity in Wistar male rats subjected to chronic psychosocial
isolation and/or treated with fluoxetine. Chronically isolated animals exhibited
decreased levels of plasma corticoserone (CORT). AOEs status was not altered either
by chronic social isolation or by fluoxetine. The only exception was GLR, whose level
and activity were both markedly reduced by fluoxetine. Our study indicates that
fluoxetine treatment of chronically isolated male Wistar rats, leads to significant
reduction in the level and activity of GLR in the erythrocytes.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry",
title = "Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9306"
}

Adžić, M., Đorđević, A. D., Đorđević, J., Elaković, I., Simić, I., Mitić, M., Rackov, G., Matić, G.,& Radojčić, M.. (2010). Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia..
https://hdl.handle.net/21.15107/rcub_vinar_9306

Adžić M, Đorđević AD, Đorđević J, Elaković I, Simić I, Mitić M, Rackov G, Matić G, Radojčić M. Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry. 2010;.
https://hdl.handle.net/21.15107/rcub_vinar_9306 .

Adžić, Miroslav, Đorđević, Ana D., Đorđević, Jelena, Elaković, Ivana, Simić, Iva, Mitić, Miloš, Rackov, Gorjana, Matić, Gordana, Radojčić, Marija, "Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats" in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry (2010),
https://hdl.handle.net/21.15107/rcub_vinar_9306 .

TY  - CONF
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Đorđević, Ana D.
AU  - Đorđević, J.
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9320
AB  - Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been
implicated in the pathophysiology of depression and stress disorders.
Glucocorticoids, key regulators of stress response, have diverse effects on cellular
processes in the hippocampus. Beside non genomic pathways, glucocorticoids
effects are mediated through activation of the glucocorticoid receptor (GR), a
ligand activated transcriptional factor that belongs to the nuclear hormone receptor
superfamily. We analysed the GR protein level both, in the cytoplasmic and
nuclear compartments in Wistar rat hippocampus, exposed to 3 week social
isolation stress upon chronic fluoxetine treatment. Under chronic stress,
corticosterone level was decreased compared to the control and treatment with
fluoxetine did not change its level significantly in stressed animals. At the
molecular level, fluoxetine significantly decreased the level of nuclear GR protein
in the brain hippocampus of the chronically stressed rats. Fluoxetine reversed the
nuclear level of GR disrupted by chronic psychosocial isolation (CPSI), but it
failed to normalize HPA axis activity.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
T1  - Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9320
ER  - 

@conference{
author = "Mitić, Miloš and Simić, Iva and Đorđević, Ana D. and Đorđević, J. and Radojčić, Marija and Adžić, Miroslav",
year = "2010",
abstract = "Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been
implicated in the pathophysiology of depression and stress disorders.
Glucocorticoids, key regulators of stress response, have diverse effects on cellular
processes in the hippocampus. Beside non genomic pathways, glucocorticoids
effects are mediated through activation of the glucocorticoid receptor (GR), a
ligand activated transcriptional factor that belongs to the nuclear hormone receptor
superfamily. We analysed the GR protein level both, in the cytoplasmic and
nuclear compartments in Wistar rat hippocampus, exposed to 3 week social
isolation stress upon chronic fluoxetine treatment. Under chronic stress,
corticosterone level was decreased compared to the control and treatment with
fluoxetine did not change its level significantly in stressed animals. At the
molecular level, fluoxetine significantly decreased the level of nuclear GR protein
in the brain hippocampus of the chronically stressed rats. Fluoxetine reversed the
nuclear level of GR disrupted by chronic psychosocial isolation (CPSI), but it
failed to normalize HPA axis activity.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry",
title = "Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9320"
}

Mitić, M., Simić, I., Đorđević, A. D., Đorđević, J., Radojčić, M.,& Adžić, M.. (2010). Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia..
https://hdl.handle.net/21.15107/rcub_vinar_9320

Mitić M, Simić I, Đorđević AD, Đorđević J, Radojčić M, Adžić M. Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry. 2010;.
https://hdl.handle.net/21.15107/rcub_vinar_9320 .

Mitić, Miloš, Simić, Iva, Đorđević, Ana D., Đorđević, J., Radojčić, Marija, Adžić, Miroslav, "Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress" in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry (2010),
https://hdl.handle.net/21.15107/rcub_vinar_9320 .

TY  - CONF
AU  - Simić, Iva
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena
AU  - Mitić, Miloš
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9323
AB  - It is known that chronic psychosocial isolation (CPSI) exerts maladaptive effect on the
hypothalamic-pituitary-adrenal (HPA) axis activity. Since the hypothalamus (HT) is a
major driver of the HPA axis activity and since glucocorticoid receptor protein (GR)
mediates HPA axis negative feedback particularly in this structure, we studied the
effect of CPSI by following the expression of GR and its chaperones hsp70 and hsp90
in HT. Our results showed that the ratios of HSPs/GR set by the CPSI were altered in
response to a novel acute stress, which indicated negative CPSI influence on GR
functions in HT.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
T1  - Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9323
ER  - 

@conference{
author = "Simić, Iva and Đorđević, Ana D. and Đorđević, Jelena and Mitić, Miloš and Radojčić, Marija and Adžić, Miroslav",
year = "2010",
abstract = "It is known that chronic psychosocial isolation (CPSI) exerts maladaptive effect on the
hypothalamic-pituitary-adrenal (HPA) axis activity. Since the hypothalamus (HT) is a
major driver of the HPA axis activity and since glucocorticoid receptor protein (GR)
mediates HPA axis negative feedback particularly in this structure, we studied the
effect of CPSI by following the expression of GR and its chaperones hsp70 and hsp90
in HT. Our results showed that the ratios of HSPs/GR set by the CPSI were altered in
response to a novel acute stress, which indicated negative CPSI influence on GR
functions in HT.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry",
title = "Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9323"
}

Simić, I., Đorđević, A. D., Đorđević, J., Mitić, M., Radojčić, M.,& Adžić, M.. (2010). Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia..
https://hdl.handle.net/21.15107/rcub_vinar_9323

Simić I, Đorđević AD, Đorđević J, Mitić M, Radojčić M, Adžić M. Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry. 2010;.
https://hdl.handle.net/21.15107/rcub_vinar_9323 .

Simić, Iva, Đorđević, Ana D., Đorđević, Jelena, Mitić, Miloš, Radojčić, Marija, Adžić, Miroslav, "Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus" in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry (2010),
https://hdl.handle.net/21.15107/rcub_vinar_9323 .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Nićiforović, Ana
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4153
AB  - Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.
T2  - Physiological Research
T1  - Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats
VL  - 59
IS  - 5
SP  - 729
EP  - 736
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4153
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Nićiforović, Ana and Radojčić, Marija",
year = "2010",
abstract = "Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.",
journal = "Physiological Research",
title = "Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats",
volume = "59",
number = "5",
pages = "729-736",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4153"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M., Nićiforović, A.,& Radojčić, M.. (2010). Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats. in Physiological Research, 59(5), 729-736.
https://hdl.handle.net/21.15107/rcub_vinar_4153

Đorđević JD, Đorđević AD, Adžić M, Nićiforović A, Radojčić M. Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats. in Physiological Research. 2010;59(5):729-736.
https://hdl.handle.net/21.15107/rcub_vinar_4153 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Nićiforović, Ana, Radojčić, Marija, "Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats" in Physiological Research, 59, no. 5 (2010):729-736,
https://hdl.handle.net/21.15107/rcub_vinar_4153 .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4060
AB  - Successful adaptation to stress involves synergized actions of glucocorticoids and catecholamines at several levels of the CNS, including the prefrontal cortex (PFC). Inside the PFC, hormonal signals trigger concerted actions of transcriptional factors, such as glucocorticoid receptor (GR) and nuclear factor kappa B (NF kappa B), culminating in a balanced, proadaptive expression of their common genes, such as proplastic NCAM and/or apoptotic Bax and Bcl-2. In the present study, we hypothesized that chronic stress may compromise the balance between GR and NF kappa B signals and lead to an altered/maladaptive expression of their cognate genes in the PFC. Our results obtained with Wistar rats exposed to chronic social isolation indicated alterations of the GR relative to the NF kappa B, in favor of the GA, in both the cytoplasmic and the nuclear compartments of the PFC. Although these alterations did not affect the induction of proplastic NCAM gene, they decreased the NCAM sialylation necessary for plastic response and caused marked relocation of the mitochondrial membrane antiapoptotic Bcl-2 protein to its cytoplasmic form. Moreover, the compromised PSA-NCAM plastic response found under chronic stress was sustained after exposure of animals to the subsequent acute stress, whereas the proapoptotic signals were further emphasized. It is concluded that chronic social isolation of Wistar animals leads to a maladaptive response of the PFC, considering the diminishment of its plastic potential and potentiating of apoptosis. Such conditions in the PFC are likely to compromise its ability to interact with other CNS structures, such as the hippocampus, which is necessary for successful adaptation to stress. (C) 2010 Wiley-Liss, Inc.
T2  - Journal of Neuroscience Research
T1  - Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats
VL  - 88
IS  - 11
SP  - 2524
EP  - 2533
DO  - 10.1002/jnr.22403
ER  - 

@article{
author = "Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radojčić, Marija",
year = "2010",
abstract = "Successful adaptation to stress involves synergized actions of glucocorticoids and catecholamines at several levels of the CNS, including the prefrontal cortex (PFC). Inside the PFC, hormonal signals trigger concerted actions of transcriptional factors, such as glucocorticoid receptor (GR) and nuclear factor kappa B (NF kappa B), culminating in a balanced, proadaptive expression of their common genes, such as proplastic NCAM and/or apoptotic Bax and Bcl-2. In the present study, we hypothesized that chronic stress may compromise the balance between GR and NF kappa B signals and lead to an altered/maladaptive expression of their cognate genes in the PFC. Our results obtained with Wistar rats exposed to chronic social isolation indicated alterations of the GR relative to the NF kappa B, in favor of the GA, in both the cytoplasmic and the nuclear compartments of the PFC. Although these alterations did not affect the induction of proplastic NCAM gene, they decreased the NCAM sialylation necessary for plastic response and caused marked relocation of the mitochondrial membrane antiapoptotic Bcl-2 protein to its cytoplasmic form. Moreover, the compromised PSA-NCAM plastic response found under chronic stress was sustained after exposure of animals to the subsequent acute stress, whereas the proapoptotic signals were further emphasized. It is concluded that chronic social isolation of Wistar animals leads to a maladaptive response of the PFC, considering the diminishment of its plastic potential and potentiating of apoptosis. Such conditions in the PFC are likely to compromise its ability to interact with other CNS structures, such as the hippocampus, which is necessary for successful adaptation to stress. (C) 2010 Wiley-Liss, Inc.",
journal = "Journal of Neuroscience Research",
title = "Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats",
volume = "88",
number = "11",
pages = "2524-2533",
doi = "10.1002/jnr.22403"
}

Đorđević, A. D., Adžić, M., Đorđević, J. D.,& Radojčić, M.. (2010). Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats. in Journal of Neuroscience Research, 88(11), 2524-2533.
https://doi.org/10.1002/jnr.22403

Đorđević AD, Adžić M, Đorđević JD, Radojčić M. Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats. in Journal of Neuroscience Research. 2010;88(11):2524-2533.
doi:10.1002/jnr.22403 .

Đorđević, Ana D., Adžić, Miroslav, Đorđević, Jelena D., Radojčić, Marija, "Chronic Social Isolation Suppresses Proplastic Response and Promotes Proapoptotic Signalling in Prefrontal Cortex of Wistar Rats" in Journal of Neuroscience Research, 88, no. 11 (2010):2524-2533,
https://doi.org/10.1002/jnr.22403 . .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Radoičić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4020
AB  - Chronic neuroendocrine stress usually leads to the elevation of the stress hormones and increased metabolic rate, which is frequently accompanied by oxidative damage to the CNS. In the present study we hypothesized that chronic psychosocial isolation (CPSI) of male Wistar rats, characterized by decreased serum corticosterone (CORT), unaltered catecholamines (CTs), and low blood glucose (GLU), may also promote oxidative imbalance in the CNS, by targeting antioxidant defense system. To test it, we have examined the relation between these input signals and protein expression/activity of antioxidant enzymes (AOEs): superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GLR) in the hippocampus (HIPPO) of CPSI animals. We found that CPSI did not affect SODs or CAT, but decreased activity of GPx and compromised GLR, an enzyme highly dependent on blood GLU for its substrate precursor. Further, we have tested whether the CPSI experience altered AOEs response to a novelty stress, and found that it attenuated peroxide-metabolizing enzymes, CAT and GPx, and decreased GLR activity, even though blood GLU was restored. The altered ratios of hippocampal AOEs in CPSI animals, which were worsened under the combined stress conditions, may lead to the accumulation of peroxide products and oxidative imbalance. The mechanism by which CPSI generate oxidative imbalance in the HIPPO is most likely based on poor systemic energy conditions set by this stress. Such conditions may cause functional decline of CNS structures, such as HIPPO, and are likely to promote state linked to onset of many mood disorders.
T2  - Cellular and Molecular Neurobiology
T1  - Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats
VL  - 30
IS  - 5
SP  - 693
EP  - 700
DO  - 10.1007/s10571-009-9493-0
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Radoičić, Marija",
year = "2010",
abstract = "Chronic neuroendocrine stress usually leads to the elevation of the stress hormones and increased metabolic rate, which is frequently accompanied by oxidative damage to the CNS. In the present study we hypothesized that chronic psychosocial isolation (CPSI) of male Wistar rats, characterized by decreased serum corticosterone (CORT), unaltered catecholamines (CTs), and low blood glucose (GLU), may also promote oxidative imbalance in the CNS, by targeting antioxidant defense system. To test it, we have examined the relation between these input signals and protein expression/activity of antioxidant enzymes (AOEs): superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GLR) in the hippocampus (HIPPO) of CPSI animals. We found that CPSI did not affect SODs or CAT, but decreased activity of GPx and compromised GLR, an enzyme highly dependent on blood GLU for its substrate precursor. Further, we have tested whether the CPSI experience altered AOEs response to a novelty stress, and found that it attenuated peroxide-metabolizing enzymes, CAT and GPx, and decreased GLR activity, even though blood GLU was restored. The altered ratios of hippocampal AOEs in CPSI animals, which were worsened under the combined stress conditions, may lead to the accumulation of peroxide products and oxidative imbalance. The mechanism by which CPSI generate oxidative imbalance in the HIPPO is most likely based on poor systemic energy conditions set by this stress. Such conditions may cause functional decline of CNS structures, such as HIPPO, and are likely to promote state linked to onset of many mood disorders.",
journal = "Cellular and Molecular Neurobiology",
title = "Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats",
volume = "30",
number = "5",
pages = "693-700",
doi = "10.1007/s10571-009-9493-0"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M.,& Radoičić, M.. (2010). Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats. in Cellular and Molecular Neurobiology, 30(5), 693-700.
https://doi.org/10.1007/s10571-009-9493-0

Đorđević JD, Đorđević AD, Adžić M, Radoičić M. Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats. in Cellular and Molecular Neurobiology. 2010;30(5):693-700.
doi:10.1007/s10571-009-9493-0 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Radoičić, Marija, "Chronic Social Isolation Compromises the Activity of Both Glutathione Peroxidase and Catalase in Hippocampus of Male Wistar Rats" in Cellular and Molecular Neurobiology, 30, no. 5 (2010):693-700,
https://doi.org/10.1007/s10571-009-9493-0 . .

TY  - JOUR
AU  - Elaković, Ivana
AU  - Vasiljević, Đorđe
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3960
AB  - Gender-related differences in the expression and functional properties of the hepatic glucocorticoid receptor were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Some of the receptors functional properties, including hormone-binding capacity (B-max), hormone-binding potency (B-max/K-D ratio) and the DNA-binding ability, were found to be sexually dimorphic. Fluoxetine treatment (5 mg/kg body mass, 21 day, intraperitoneally) induced a decrease in B-max and in the amount of Hsp70 co-immunoprecipitated with the glucocorticoid receptor only in males, and stimulated the association of the receptor with Hsp90 in females. When applied during the last three weeks of the 6-week isolation, fluoxetine parallelly elevated B-max and the receptor protein level in female animals, while in males diminished B-max and inhibited association of the receptor with Hsp70. Binding of dexamethasone-receptor complexes both to DNA-cellulose and to isolated liver nuclei did not appear to be a target for fluoxetine action. The results point to sex-related differences in the glucocorticoid receptor functioning and in its response to fluoxetine, and suggest that these differences may contribute to well known sexual dimorphism in the sensitivity to stress, to stress-related disorders and to antidepressant treatment. (C) 2010 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine
VL  - 632
IS  - 1-3
SP  - 79
EP  - 85
DO  - 10.1016/j.ejphar.2010.01.015
ER  - 

@article{
author = "Elaković, Ivana and Vasiljević, Đorđe and Adžić, Miroslav and Đorđević, Ana D. and Đorđević, Jelena D. and Matić, Gordana and Radojčić, Marija",
year = "2010",
abstract = "Gender-related differences in the expression and functional properties of the hepatic glucocorticoid receptor were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Some of the receptors functional properties, including hormone-binding capacity (B-max), hormone-binding potency (B-max/K-D ratio) and the DNA-binding ability, were found to be sexually dimorphic. Fluoxetine treatment (5 mg/kg body mass, 21 day, intraperitoneally) induced a decrease in B-max and in the amount of Hsp70 co-immunoprecipitated with the glucocorticoid receptor only in males, and stimulated the association of the receptor with Hsp90 in females. When applied during the last three weeks of the 6-week isolation, fluoxetine parallelly elevated B-max and the receptor protein level in female animals, while in males diminished B-max and inhibited association of the receptor with Hsp70. Binding of dexamethasone-receptor complexes both to DNA-cellulose and to isolated liver nuclei did not appear to be a target for fluoxetine action. The results point to sex-related differences in the glucocorticoid receptor functioning and in its response to fluoxetine, and suggest that these differences may contribute to well known sexual dimorphism in the sensitivity to stress, to stress-related disorders and to antidepressant treatment. (C) 2010 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine",
volume = "632",
number = "1-3",
pages = "79-85",
doi = "10.1016/j.ejphar.2010.01.015"
}

Elaković, I., Vasiljević, Đ., Adžić, M., Đorđević, A. D., Đorđević, J. D., Matić, G.,& Radojčić, M.. (2010). Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine. in European Journal of Pharmacology, 632(1-3), 79-85.
https://doi.org/10.1016/j.ejphar.2010.01.015

Elaković I, Vasiljević Đ, Adžić M, Đorđević AD, Đorđević JD, Matić G, Radojčić M. Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine. in European Journal of Pharmacology. 2010;632(1-3):79-85.
doi:10.1016/j.ejphar.2010.01.015 .

Elaković, Ivana, Vasiljević, Đorđe, Adžić, Miroslav, Đorđević, Ana D., Đorđević, Jelena D., Matić, Gordana, Radojčić, Marija, "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine" in European Journal of Pharmacology, 632, no. 1-3 (2010):79-85,
https://doi.org/10.1016/j.ejphar.2010.01.015 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Nićiforović, Ana
AU  - Demonacos, Constantinos
AU  - Radoičić, Marija B.
AU  - Krstić-Demonacos, Marija
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3848
AB  - Chronic stress and impaired glucocorticoid receptor (GR) feedback are important factors for the compromised hypothalamic-pituitary-adrenal (HPA) axis activity. We investigated the effects of chronic 2 1 day isolation of Wistar rats on the extrinsic negative feedback part of I-IPA axis: hippocampus (HIPPO) and prefrontal cortex (PFC). In addition to serum corticosterone (CORT), we followed GR subcellular localization, GR phosphorylation at serine 232 and serine 246, expression of GR, regulated genes: GR, CRF and brain-derived neurotropic factor (BDNF), and activity of c-Jun N-terminal kinase (JNK) and Cdk5 kinases that phosphorylate GR. These parameters were also determined in animals subjected to acute 30 min immobilization, which was taken as normal adaptive response to stress. In isolated animals, we found decreased CORT, whereas, in animals exposed to acute immobilization, CORT was markedly increased. Even though the GR was predominantly localized in the nucleus of HIPPO and PFC in acute, but not in chronic stress, the expression of GR, CRF, and BDNF genes was similarly regulated under both acute and chronic stresses. Thus, the transcriptional activity of GR under chronic isolation did not seem to be exclusively dependent on high serum CORT levels nor on the subcellular location of the GR protein. Rather, it resulted front the increased Cdk5 activation and phosphorylation of the nuclear GR at serine 232 and the decreased JNK activity reflected in decreased phosphorylation of the nuclear GR at serine 246. Our study suggests that this nuclear isoform of hippocampal and cortical GR may be related to hypocorticism i.e. HPA axis hypoactivity under chronic isolation stress. journal of Endocrinology (2009) 202, 87-97
T2  - Journal of Endocrinology
T1  - Acute or chronic stress induce cell compartment-specific phosphorylation of glucocorticoid receptor and alter its transcriptional activity in Wistar rat brain
VL  - 202
IS  - 1
SP  - 87
EP  - 97
DO  - 10.1677/JOE-08-0509
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Đorđević, Ana D. and Nićiforović, Ana and Demonacos, Constantinos and Radoičić, Marija B. and Krstić-Demonacos, Marija",
year = "2009",
abstract = "Chronic stress and impaired glucocorticoid receptor (GR) feedback are important factors for the compromised hypothalamic-pituitary-adrenal (HPA) axis activity. We investigated the effects of chronic 2 1 day isolation of Wistar rats on the extrinsic negative feedback part of I-IPA axis: hippocampus (HIPPO) and prefrontal cortex (PFC). In addition to serum corticosterone (CORT), we followed GR subcellular localization, GR phosphorylation at serine 232 and serine 246, expression of GR, regulated genes: GR, CRF and brain-derived neurotropic factor (BDNF), and activity of c-Jun N-terminal kinase (JNK) and Cdk5 kinases that phosphorylate GR. These parameters were also determined in animals subjected to acute 30 min immobilization, which was taken as normal adaptive response to stress. In isolated animals, we found decreased CORT, whereas, in animals exposed to acute immobilization, CORT was markedly increased. Even though the GR was predominantly localized in the nucleus of HIPPO and PFC in acute, but not in chronic stress, the expression of GR, CRF, and BDNF genes was similarly regulated under both acute and chronic stresses. Thus, the transcriptional activity of GR under chronic isolation did not seem to be exclusively dependent on high serum CORT levels nor on the subcellular location of the GR protein. Rather, it resulted front the increased Cdk5 activation and phosphorylation of the nuclear GR at serine 232 and the decreased JNK activity reflected in decreased phosphorylation of the nuclear GR at serine 246. Our study suggests that this nuclear isoform of hippocampal and cortical GR may be related to hypocorticism i.e. HPA axis hypoactivity under chronic isolation stress. journal of Endocrinology (2009) 202, 87-97",
journal = "Journal of Endocrinology",
title = "Acute or chronic stress induce cell compartment-specific phosphorylation of glucocorticoid receptor and alter its transcriptional activity in Wistar rat brain",
volume = "202",
number = "1",
pages = "87-97",
doi = "10.1677/JOE-08-0509"
}

Adžić, M., Đorđević, J. D., Đorđević, A. D., Nićiforović, A., Demonacos, C., Radoičić, M. B.,& Krstić-Demonacos, M.. (2009). Acute or chronic stress induce cell compartment-specific phosphorylation of glucocorticoid receptor and alter its transcriptional activity in Wistar rat brain. in Journal of Endocrinology, 202(1), 87-97.
https://doi.org/10.1677/JOE-08-0509

Adžić M, Đorđević JD, Đorđević AD, Nićiforović A, Demonacos C, Radoičić MB, Krstić-Demonacos M. Acute or chronic stress induce cell compartment-specific phosphorylation of glucocorticoid receptor and alter its transcriptional activity in Wistar rat brain. in Journal of Endocrinology. 2009;202(1):87-97.
doi:10.1677/JOE-08-0509 .

Adžić, Miroslav, Đorđević, Jelena D., Đorđević, Ana D., Nićiforović, Ana, Demonacos, Constantinos, Radoičić, Marija B., Krstić-Demonacos, Marija, "Acute or chronic stress induce cell compartment-specific phosphorylation of glucocorticoid receptor and alter its transcriptional activity in Wistar rat brain" in Journal of Endocrinology, 202, no. 1 (2009):87-97,
https://doi.org/10.1677/JOE-08-0509 . .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3822
AB  - Successful adaptation to stress involves actions of glucocorticoid receptor (GR), a steroid-dependent transcription factor, abundant in hippocampus. Another transcription factor, nuclear factor kappa B (NF kappa B) is considered as an important stress sensor implicated in adaptive synaptic plasticity. Numerous stress-related genes are regulated by both hippocampal GR and NF kappa B, including neural cell adhesion molecules (NCAM and L1), involved in plasticity, and genes that encode apoptotic proteins (bax and bcl-2). We presumed that the ratio of nuclear NF kappa B to nuclear GR may determine the degree of proplastic or proapoptotic signaling under stress. To test this presumption we have investigated effects of acute, chronic and combined stress on compartmental levels and ratios of NF kappa B and GR proteins, and in parallel, changes in their mRNA expression. In addition, the expression of plasticity (NCAM, L1) and apoptotic (bax, bcl-2) genes, as well as, Bax and Bcl-2 proteins redistribution between mitochondrial and cytoplasmic compartments, were followed. When glucocorticoid levels were low, as found in chronic stress, GR was not efficiently translocated to the nucleus. This resulted in its lower nuclear level relative to the nuclear NF kappa B. Such conditions did not affect proplastic induction of NCAM mRNA, but were related to the onset of proapoptotic signaling illustrated by relocation of mitochondrial Bcl-2 protein to its soluble cytoplasmic form. Because these Bcl-2 rearrangements were not reversed by subsequent acute stress, representing more stable alterations, it is concluded that chronic social isolation of Wistar rats led to the initiation of proapoptotic signaling that may be etiologically related to compromised adaptive response of central nervous system.
T2  - Journal of Neural Transmission
T1  - Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus
VL  - 116
IS  - 12
SP  - 1579
EP  - 1589
DO  - 10.1007/s00702-009-0286-x
ER  - 

@article{
author = "Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radojčić, Marija",
year = "2009",
abstract = "Successful adaptation to stress involves actions of glucocorticoid receptor (GR), a steroid-dependent transcription factor, abundant in hippocampus. Another transcription factor, nuclear factor kappa B (NF kappa B) is considered as an important stress sensor implicated in adaptive synaptic plasticity. Numerous stress-related genes are regulated by both hippocampal GR and NF kappa B, including neural cell adhesion molecules (NCAM and L1), involved in plasticity, and genes that encode apoptotic proteins (bax and bcl-2). We presumed that the ratio of nuclear NF kappa B to nuclear GR may determine the degree of proplastic or proapoptotic signaling under stress. To test this presumption we have investigated effects of acute, chronic and combined stress on compartmental levels and ratios of NF kappa B and GR proteins, and in parallel, changes in their mRNA expression. In addition, the expression of plasticity (NCAM, L1) and apoptotic (bax, bcl-2) genes, as well as, Bax and Bcl-2 proteins redistribution between mitochondrial and cytoplasmic compartments, were followed. When glucocorticoid levels were low, as found in chronic stress, GR was not efficiently translocated to the nucleus. This resulted in its lower nuclear level relative to the nuclear NF kappa B. Such conditions did not affect proplastic induction of NCAM mRNA, but were related to the onset of proapoptotic signaling illustrated by relocation of mitochondrial Bcl-2 protein to its soluble cytoplasmic form. Because these Bcl-2 rearrangements were not reversed by subsequent acute stress, representing more stable alterations, it is concluded that chronic social isolation of Wistar rats led to the initiation of proapoptotic signaling that may be etiologically related to compromised adaptive response of central nervous system.",
journal = "Journal of Neural Transmission",
title = "Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus",
volume = "116",
number = "12",
pages = "1579-1589",
doi = "10.1007/s00702-009-0286-x"
}

Đorđević, A. D., Adžić, M., Đorđević, J. D.,& Radojčić, M.. (2009). Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus. in Journal of Neural Transmission, 116(12), 1579-1589.
https://doi.org/10.1007/s00702-009-0286-x

Đorđević AD, Adžić M, Đorđević JD, Radojčić M. Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus. in Journal of Neural Transmission. 2009;116(12):1579-1589.
doi:10.1007/s00702-009-0286-x .

Đorđević, Ana D., Adžić, Miroslav, Đorđević, Jelena D., Radojčić, Marija, "Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus" in Journal of Neural Transmission, 116, no. 12 (2009):1579-1589,
https://doi.org/10.1007/s00702-009-0286-x . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Demonacos, Constantinos
AU  - Krstić-Demonacos, Marija
AU  - Radojčić, Marija
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3810
AB  - Mitochondrial dysfunction is increasingly recognized as a key component in compromised neuroendocrine stress response and. among other etiological causes. it may also involve action of glucocorticoid hormones. In the current study we followed glucocorticoid receptor and Identified its mitochondrial phosphoisophorms in hippocampus and prefrontal brain cortex of Wistar male rats subjected to acute. chronic and combined neuroendocrine stresses. In both brain structures chronic social isolation caused m,irked increase in mitochondrial glucocorticoid receptor that was preferentially phosphorylated at serine 232 compared to serine 246 or serine 171. This increase corresponded with the decreased expression of mitochondrially encoded cytochrome oxidase subunits 1 and 3 in hippocampus, and with their increased expression in prefrontal brain cortex. Prefrontal brain cortex appeared to be more sensitive to chronic stress, since it exibited higher levels of mitochondrial Bax and cytoplasmic Bcl2 compared to hippocampus. Chronic stress also altered the response of both brain structures to subsequent acute stress according to the studied parameters. Therefore, prolonged social isolation may cause susceptibility to mitochondria triggered proapototic signalling. which at least in part may be mediated by the glucocorticoid receptor dependent mechanism. (C) 2009 Elsevier Ltd All rights reserved.
T2  - International Journal of Biochemistry and Cell Biology
T1  - The role of phosphorylated glucocorticoid receptor in mitochondrial functions and apoptotic signalling in brain tissue of stressed Wistar rats
VL  - 41
IS  - 11
SP  - 2181
EP  - 2188
DO  - 10.1016/j.biocel.2009.04.001
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Ana D. and Demonacos, Constantinos and Krstić-Demonacos, Marija and Radojčić, Marija",
year = "2009",
abstract = "Mitochondrial dysfunction is increasingly recognized as a key component in compromised neuroendocrine stress response and. among other etiological causes. it may also involve action of glucocorticoid hormones. In the current study we followed glucocorticoid receptor and Identified its mitochondrial phosphoisophorms in hippocampus and prefrontal brain cortex of Wistar male rats subjected to acute. chronic and combined neuroendocrine stresses. In both brain structures chronic social isolation caused m,irked increase in mitochondrial glucocorticoid receptor that was preferentially phosphorylated at serine 232 compared to serine 246 or serine 171. This increase corresponded with the decreased expression of mitochondrially encoded cytochrome oxidase subunits 1 and 3 in hippocampus, and with their increased expression in prefrontal brain cortex. Prefrontal brain cortex appeared to be more sensitive to chronic stress, since it exibited higher levels of mitochondrial Bax and cytoplasmic Bcl2 compared to hippocampus. Chronic stress also altered the response of both brain structures to subsequent acute stress according to the studied parameters. Therefore, prolonged social isolation may cause susceptibility to mitochondria triggered proapototic signalling. which at least in part may be mediated by the glucocorticoid receptor dependent mechanism. (C) 2009 Elsevier Ltd All rights reserved.",
journal = "International Journal of Biochemistry and Cell Biology",
title = "The role of phosphorylated glucocorticoid receptor in mitochondrial functions and apoptotic signalling in brain tissue of stressed Wistar rats",
volume = "41",
number = "11",
pages = "2181-2188",
doi = "10.1016/j.biocel.2009.04.001"
}

Adžić, M., Đorđević, A. D., Demonacos, C., Krstić-Demonacos, M.,& Radojčić, M.. (2009). The role of phosphorylated glucocorticoid receptor in mitochondrial functions and apoptotic signalling in brain tissue of stressed Wistar rats. in International Journal of Biochemistry and Cell Biology, 41(11), 2181-2188.
https://doi.org/10.1016/j.biocel.2009.04.001

Adžić M, Đorđević AD, Demonacos C, Krstić-Demonacos M, Radojčić M. The role of phosphorylated glucocorticoid receptor in mitochondrial functions and apoptotic signalling in brain tissue of stressed Wistar rats. in International Journal of Biochemistry and Cell Biology. 2009;41(11):2181-2188.
doi:10.1016/j.biocel.2009.04.001 .

Adžić, Miroslav, Đorđević, Ana D., Demonacos, Constantinos, Krstić-Demonacos, Marija, Radojčić, Marija, "The role of phosphorylated glucocorticoid receptor in mitochondrial functions and apoptotic signalling in brain tissue of stressed Wistar rats" in International Journal of Biochemistry and Cell Biology, 41, no. 11 (2009):2181-2188,
https://doi.org/10.1016/j.biocel.2009.04.001 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Krstić-Demonacos, Marija
AU  - Radoičić, Marija B.
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3785
AB  - In the paper entitled: Adžić, M., Đorđević, A., Krstić-Demonacos, M., & Radojčić, M. B. (2009). Stress-induced phosphorylation of c-Jun-N-terminal kinases and nuclear translocation of Hsp70 in the Wistar rat hippocampus. Archives of Biological Sciences, 61(1), 1-8.

Fig. 1, on page 4, section b, should read "Nucleus" instead of "Cytoplasm"
T2  - Archives of Biological Sciences
T1  - Errata Corrige "Stress-Induced phosphorylation of C-JUN-N-Terminal kinases and nuclear translocation of HSP70 in the wistar rat hippocampus" [Arch. Biol. Sci. Belgrade 61(1) (2009) 1-8, DOI: 10.2298/ABS0901001A]
VL  - 61
IS  - 3
SP  - 571
UR  - https://hdl.handle.net/21.15107/rcub_vinar_3785
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Ana D. and Krstić-Demonacos, Marija and Radoičić, Marija B.",
year = "2009",
abstract = "In the paper entitled: Adžić, M., Đorđević, A., Krstić-Demonacos, M., & Radojčić, M. B. (2009). Stress-induced phosphorylation of c-Jun-N-terminal kinases and nuclear translocation of Hsp70 in the Wistar rat hippocampus. Archives of Biological Sciences, 61(1), 1-8.

Fig. 1, on page 4, section b, should read "Nucleus" instead of "Cytoplasm"",
journal = "Archives of Biological Sciences",
title = "Errata Corrige "Stress-Induced phosphorylation of C-JUN-N-Terminal kinases and nuclear translocation of HSP70 in the wistar rat hippocampus" [Arch. Biol. Sci. Belgrade 61(1) (2009) 1-8, DOI: 10.2298/ABS0901001A]",
volume = "61",
number = "3",
pages = "571",
url = "https://hdl.handle.net/21.15107/rcub_vinar_3785"
}

Adžić, M., Đorđević, A. D., Krstić-Demonacos, M.,& Radoičić, M. B.. (2009). Errata Corrige "Stress-Induced phosphorylation of C-JUN-N-Terminal kinases and nuclear translocation of HSP70 in the wistar rat hippocampus" [Arch. Biol. Sci. Belgrade 61(1) (2009) 1-8, DOI: 10.2298/ABS0901001A]. in Archives of Biological Sciences, 61(3), 571.
https://hdl.handle.net/21.15107/rcub_vinar_3785

Adžić M, Đorđević AD, Krstić-Demonacos M, Radoičić MB. Errata Corrige "Stress-Induced phosphorylation of C-JUN-N-Terminal kinases and nuclear translocation of HSP70 in the wistar rat hippocampus" [Arch. Biol. Sci. Belgrade 61(1) (2009) 1-8, DOI: 10.2298/ABS0901001A]. in Archives of Biological Sciences. 2009;61(3):571.
https://hdl.handle.net/21.15107/rcub_vinar_3785 .

Adžić, Miroslav, Đorđević, Ana D., Krstić-Demonacos, Marija, Radoičić, Marija B., "Errata Corrige "Stress-Induced phosphorylation of C-JUN-N-Terminal kinases and nuclear translocation of HSP70 in the wistar rat hippocampus" [Arch. Biol. Sci. Belgrade 61(1) (2009) 1-8, DOI: 10.2298/ABS0901001A]" in Archives of Biological Sciences, 61, no. 3 (2009):571,
https://hdl.handle.net/21.15107/rcub_vinar_3785 .