Matić, Gordana

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orcid::0000-0002-0142-1056
  • Matić, Gordana (19)

Author's Bibliography

PTSD and depressive symptoms are linked to DHEAS via personality

Savić, Danka A.; Knežević, Goran; Matić, Gordana; Damjanović, Svetozar S.

(2018)

TY  - JOUR
AU  - Savić, Danka A.
AU  - Knežević, Goran
AU  - Matić, Gordana
AU  - Damjanović, Svetozar S.
PY  - 2018
UR  - http://linkinghub.elsevier.com/retrieve/pii/S030645301830088X
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/7745
AB  - Background Research results on dehydroepiandrosterone sulfate ester (DHEAS) in post-traumatic stress disorder (PTSD) are inconsistent. We hypothesized that personality traits could be the confounders of DHEAS levels and disease symptoms, which could in part explain the discrepancy in findings. Method: This study was a part of a broader project in which simultaneous psychological and biological in-vestigations were carried out in hospital conditions. 380 male subjects were categorized in four groups: A) current PTSD (n = 132), B) lifetime PTSD (n = 66), C) trauma controls (n = 101), and D) healthy controls (n = 81), matched by age. Results: The level of DHEAS is significantly lower in the current PTSD group than in trauma controls. All groups significantly differ in personality traits Disintegration and Neuroticism (current PTSD group having the highest scores). DHEAS is related to both PTSD and depressive symptoms; however, Structural Equation Model (SEM) shows that the relations are indirect, realized via their confounder-personality trait Disintegration. Conclusions: According to our project results, DHEAS is the second putative biomarker for trauma-related dis-orders that fails to fulfil this expectation. It appears to be more directly related to personality than to the disease symptoms (the first one being basal cortisol). Our data promote personality as a biologically based construct with seemingly important role in understanding the mental health status.
T2  - Psychoneuroendocrinology
T1  - PTSD and depressive symptoms are linked to DHEAS via personality
VL  - 92
SP  - 29
EP  - 33
DO  - 10.1016/j.psyneuen.2018.03.017
ER  - 
@article{
author = "Savić, Danka A. and Knežević, Goran and Matić, Gordana and Damjanović, Svetozar S.",
year = "2018",
url = "http://linkinghub.elsevier.com/retrieve/pii/S030645301830088X, http://vinar.vin.bg.ac.rs/handle/123456789/7745",
abstract = "Background Research results on dehydroepiandrosterone sulfate ester (DHEAS) in post-traumatic stress disorder (PTSD) are inconsistent. We hypothesized that personality traits could be the confounders of DHEAS levels and disease symptoms, which could in part explain the discrepancy in findings. Method: This study was a part of a broader project in which simultaneous psychological and biological in-vestigations were carried out in hospital conditions. 380 male subjects were categorized in four groups: A) current PTSD (n = 132), B) lifetime PTSD (n = 66), C) trauma controls (n = 101), and D) healthy controls (n = 81), matched by age. Results: The level of DHEAS is significantly lower in the current PTSD group than in trauma controls. All groups significantly differ in personality traits Disintegration and Neuroticism (current PTSD group having the highest scores). DHEAS is related to both PTSD and depressive symptoms; however, Structural Equation Model (SEM) shows that the relations are indirect, realized via their confounder-personality trait Disintegration. Conclusions: According to our project results, DHEAS is the second putative biomarker for trauma-related dis-orders that fails to fulfil this expectation. It appears to be more directly related to personality than to the disease symptoms (the first one being basal cortisol). Our data promote personality as a biologically based construct with seemingly important role in understanding the mental health status.",
journal = "Psychoneuroendocrinology",
title = "PTSD and depressive symptoms are linked to DHEAS via personality",
volume = "92",
pages = "29-33",
doi = "10.1016/j.psyneuen.2018.03.017"
}
Savić, D. A., Knežević, G., Matić, G.,& Damjanović, S. S. (2018). PTSD and depressive symptoms are linked to DHEAS via personality.
Psychoneuroendocrinology, 92, 29-33.
https://doi.org/10.1016/j.psyneuen.2018.03.017
Savić DA, Knežević G, Matić G, Damjanović SS. PTSD and depressive symptoms are linked to DHEAS via personality. Psychoneuroendocrinology. 2018;92:29-33
Savić Danka A., Knežević Goran, Matić Gordana, Damjanović Svetozar S., "PTSD and depressive symptoms are linked to DHEAS via personality" Psychoneuroendocrinology, 92 (2018):29-33,
https://doi.org/10.1016/j.psyneuen.2018.03.017 .
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Posttraumatic and depressive symptoms in beta-endorphin dynamics

Savić, Danka A.; Knežević, Goran; Matić, Gordana; Damjanović, Svetozar S.; Spiric, Zeljko

(2015)

TY  - JOUR
AU  - Savić, Danka A.
AU  - Knežević, Goran
AU  - Matić, Gordana
AU  - Damjanović, Svetozar S.
AU  - Spiric, Zeljko
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/554
AB  - A disturbed beta-endorphin system can be a part of the post-traumatic stress disorder (PTSD) and depression allostasis. Study subjects (N=392) included those with PTSD and/or (stress-induced) depression, and healthy controls with and without traumas. The aim of the study was to examine the network of relations centered around plasma beta-endorphin. The network included anxiety (as a personality trait), traumatic events, pain, aggressiveness, depressive symptoms, and three clusters of PTSD symptoms: intrusions, avoidance, and hyperarousal. Beta-endorphin was represented by individual mean from 13 time points (BEmean), reflecting the total amount of the peripherally secreted hormone, and the coefficient of variation (BEvar), calculated as the ratio of standard deviation to the mean, reflecting the hormones dynamics. BEvar correlated with all other variables, BEmean had no correlations. Structural equation modeling (SEM) was used to examine all interrelations (including their directions) of BEvar and the state/trait variables in the context of their entirety. The model revealed that hyperarousal and anxiety were the only direct agents of peripheral beta-endorphin fluctuations, mediating the effects of other variables. Traumatic events and intrusions act on BEvar via hyperarousal, while depressive symptoms, avoidance, and pain act via anxiety. Hyperarousal should be emphasized as the main agent not only because its effect on BEvar is larger than that of anxiety, but also because it increases anxiety itself (via avoidance and pain). All influences on BEvar are positive and they indicate long-term (sensitizing) effects (as opposed to direct stimulation, for example, by acute pain, anger, etc.). Relations apart from beta-endorphin are also discussed. (C) 2015 Elsevier B.V. All rights reserved,
T2  - Journal of Affective Disorders
T1  - Posttraumatic and depressive symptoms in beta-endorphin dynamics
VL  - 181
SP  - 61
EP  - 66
DO  - 10.1016/j.jad.2015.03.063
ER  - 
@article{
author = "Savić, Danka A. and Knežević, Goran and Matić, Gordana and Damjanović, Svetozar S. and Spiric, Zeljko",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/554",
abstract = "A disturbed beta-endorphin system can be a part of the post-traumatic stress disorder (PTSD) and depression allostasis. Study subjects (N=392) included those with PTSD and/or (stress-induced) depression, and healthy controls with and without traumas. The aim of the study was to examine the network of relations centered around plasma beta-endorphin. The network included anxiety (as a personality trait), traumatic events, pain, aggressiveness, depressive symptoms, and three clusters of PTSD symptoms: intrusions, avoidance, and hyperarousal. Beta-endorphin was represented by individual mean from 13 time points (BEmean), reflecting the total amount of the peripherally secreted hormone, and the coefficient of variation (BEvar), calculated as the ratio of standard deviation to the mean, reflecting the hormones dynamics. BEvar correlated with all other variables, BEmean had no correlations. Structural equation modeling (SEM) was used to examine all interrelations (including their directions) of BEvar and the state/trait variables in the context of their entirety. The model revealed that hyperarousal and anxiety were the only direct agents of peripheral beta-endorphin fluctuations, mediating the effects of other variables. Traumatic events and intrusions act on BEvar via hyperarousal, while depressive symptoms, avoidance, and pain act via anxiety. Hyperarousal should be emphasized as the main agent not only because its effect on BEvar is larger than that of anxiety, but also because it increases anxiety itself (via avoidance and pain). All influences on BEvar are positive and they indicate long-term (sensitizing) effects (as opposed to direct stimulation, for example, by acute pain, anger, etc.). Relations apart from beta-endorphin are also discussed. (C) 2015 Elsevier B.V. All rights reserved,",
journal = "Journal of Affective Disorders",
title = "Posttraumatic and depressive symptoms in beta-endorphin dynamics",
volume = "181",
pages = "61-66",
doi = "10.1016/j.jad.2015.03.063"
}
Savić, D. A., Knežević, G., Matić, G., Damjanović, S. S.,& Spiric, Z. (2015). Posttraumatic and depressive symptoms in beta-endorphin dynamics.
Journal of Affective Disorders, 181, 61-66.
https://doi.org/10.1016/j.jad.2015.03.063
Savić DA, Knežević G, Matić G, Damjanović SS, Spiric Z. Posttraumatic and depressive symptoms in beta-endorphin dynamics. Journal of Affective Disorders. 2015;181:61-66
Savić Danka A., Knežević Goran, Matić Gordana, Damjanović Svetozar S., Spiric Zeljko, "Posttraumatic and depressive symptoms in beta-endorphin dynamics" Journal of Affective Disorders, 181 (2015):61-66,
https://doi.org/10.1016/j.jad.2015.03.063 .
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Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome

Tepavčević, Snežana; Milutinovic, Danijela Vojnovic; Macut, Djuro; Stojiljković, Mojca D.; Nikolic, Marina; Bozic-Antic, Ivana; Ćulafić, Tijana; Bjekic-Macut, Jelica; Matić, Gordana; Korićanac, Goran

(2015)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, Danijela Vojnovic
AU  - Macut, Djuro
AU  - Stojiljković, Mojca D.
AU  - Nikolic, Marina
AU  - Bozic-Antic, Ivana
AU  - Ćulafić, Tijana
AU  - Bjekic-Macut, Jelica
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/710
AB  - Polycystic ovary syndrome (PCOS) is associated with an altered plasma lipid profile and increased risk for cardiovascular diseases. We hypothesized that molecular mechanisms underlying cardiac pathology in PCOS involve changes in expression and subcellular localization of several key proteins involved in cardiac lipid transport and metabolism, such as fatty acid transporter CD36, lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1), and carnitine palmitoyltransferase 1 (CPT1). We used the animal model of PCOS obtained by treating female rats with dihydrotestosterone (DHT). Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative enzymes were assessed by Western blot in different cardiac cell compartments. Cardiac triglycerides (TG) and lipid peroxidation were also measured. The content of CD36 was decreased in both the cardiac plasma membranes and intracellular pool. On the other hand, total content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast to decreased microsomal lipin 1 content. An increase in nuclear content of lipin 1 was observed together with elevation of nuclear PPAR alpha and PGC1, and an increase in CPT1 expression. However, lipid peroxidation was reduced in the heart, without alterations in antioxidative enzymes expression and cardiac TG content. The results indicate that treatment of female rats with DHT is accompanied by a decrease of fatty acid uptake and a reduction of lipid peroxidation in the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.
T2  - Endocrine
T1  - Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome
VL  - 50
IS  - 1
SP  - 193
EP  - 201
DO  - 10.1007/s12020-015-0558-1
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, Danijela Vojnovic and Macut, Djuro and Stojiljković, Mojca D. and Nikolic, Marina and Bozic-Antic, Ivana and Ćulafić, Tijana and Bjekic-Macut, Jelica and Matić, Gordana and Korićanac, Goran",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/710",
abstract = "Polycystic ovary syndrome (PCOS) is associated with an altered plasma lipid profile and increased risk for cardiovascular diseases. We hypothesized that molecular mechanisms underlying cardiac pathology in PCOS involve changes in expression and subcellular localization of several key proteins involved in cardiac lipid transport and metabolism, such as fatty acid transporter CD36, lipin 1, peroxisome proliferator-activated receptor alpha (PPAR alpha), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1), and carnitine palmitoyltransferase 1 (CPT1). We used the animal model of PCOS obtained by treating female rats with dihydrotestosterone (DHT). Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative enzymes were assessed by Western blot in different cardiac cell compartments. Cardiac triglycerides (TG) and lipid peroxidation were also measured. The content of CD36 was decreased in both the cardiac plasma membranes and intracellular pool. On the other hand, total content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast to decreased microsomal lipin 1 content. An increase in nuclear content of lipin 1 was observed together with elevation of nuclear PPAR alpha and PGC1, and an increase in CPT1 expression. However, lipid peroxidation was reduced in the heart, without alterations in antioxidative enzymes expression and cardiac TG content. The results indicate that treatment of female rats with DHT is accompanied by a decrease of fatty acid uptake and a reduction of lipid peroxidation in the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1 expression suggests that cardiac fatty acid metabolism is shifted toward mitochondrial beta oxidation.",
journal = "Endocrine",
title = "Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome",
volume = "50",
number = "1",
pages = "193-201",
doi = "10.1007/s12020-015-0558-1"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Stojiljković, M. D., Nikolic, M., Bozic-Antic, I., Ćulafić, T., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2015). Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome.
Endocrine, 50(1), 193-201.
https://doi.org/10.1007/s12020-015-0558-1
Tepavčević S, Milutinovic DV, Macut D, Stojiljković MD, Nikolic M, Bozic-Antic I, Ćulafić T, Bjekic-Macut J, Matić G, Korićanac G. Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome. Endocrine. 2015;50(1):193-201
Tepavčević Snežana, Milutinovic Danijela Vojnovic, Macut Djuro, Stojiljković Mojca D., Nikolic Marina, Bozic-Antic Ivana, Ćulafić Tijana, Bjekic-Macut Jelica, Matić Gordana, Korićanac Goran, "Cardiac fatty acid uptake and metabolism in the rat model of polycystic ovary syndrome" Endocrine, 50, no. 1 (2015):193-201,
https://doi.org/10.1007/s12020-015-0558-1 .
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Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone

Tepavčević, Snežana; Milutinovic, D. V.; Macut, D.; Stanišić, Jelena; Nikolic, M.; Bozic-Antic, I.; Rodaljevic, S.; Bjekic-Macut, J.; Matić, Gordana; Korićanac, Goran

(2015)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, D. V.
AU  - Macut, D.
AU  - Stanišić, Jelena
AU  - Nikolic, M.
AU  - Bozic-Antic, I.
AU  - Rodaljevic, S.
AU  - Bjekic-Macut, J.
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/553
AB  - Nitric oxide synthases (NOSs) and Na+/K+-ATPase are enzymes essential for regular functioning of the heart. Since both enzymes are under insulin and androgen regulation and since insulin action and androgen level were disturbed in polycystic ovary syndrome (PCOS), we hypothesized that cardiac nitric oxide (NO) production and sodium/potassium transport would be deteriorated in PCOS. To test our hypothesis we introduced animal model of PCOS based on dihydrotestosterone (DHT) treatment of female Wistar rats and analyzed protein expression, phosphorylation or subcellular localization of endothelial NOS (eNOS), inducible NOS (iNOS) and alpha subunits of Na+/K+-ATPase in the heart. Obtained results indicate that DHT treatment significantly decreased cardiac eNOS protein level and activating phosphorylation at serine 1177, while inhibitory phosphorylation at threonine 495 was increased. In contrast to expression of eNOS, iNOS protein level in the heart of DHT-treated rats was significantly elevated. Furthermore, cardiac protein level of alpha 1 subunit of the ATPase, as well as its plasma membrane content, were decreased in rats with PCOS. In line with this, alpha 2 subunit protein level in fraction of plasma membranes was also significantly below control level. In conclusion, DHT treatment impaired effectiveness of NOSs and Na+/K+-ATPase in the female rat heart. Regarding the importance of NO production and sodium/potassium transport in the cardiac contraction and blood flow regulation, it implicates strong consequences of PCOS for heart functioning.
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone
VL  - 123
IS  - 5
SP  - 303
EP  - 307
DO  - 10.1055/s-0035-1548929
ER  - 
@article{
author = "Tepavčević, Snežana and Milutinovic, D. V. and Macut, D. and Stanišić, Jelena and Nikolic, M. and Bozic-Antic, I. and Rodaljevic, S. and Bjekic-Macut, J. and Matić, Gordana and Korićanac, Goran",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/553",
abstract = "Nitric oxide synthases (NOSs) and Na+/K+-ATPase are enzymes essential for regular functioning of the heart. Since both enzymes are under insulin and androgen regulation and since insulin action and androgen level were disturbed in polycystic ovary syndrome (PCOS), we hypothesized that cardiac nitric oxide (NO) production and sodium/potassium transport would be deteriorated in PCOS. To test our hypothesis we introduced animal model of PCOS based on dihydrotestosterone (DHT) treatment of female Wistar rats and analyzed protein expression, phosphorylation or subcellular localization of endothelial NOS (eNOS), inducible NOS (iNOS) and alpha subunits of Na+/K+-ATPase in the heart. Obtained results indicate that DHT treatment significantly decreased cardiac eNOS protein level and activating phosphorylation at serine 1177, while inhibitory phosphorylation at threonine 495 was increased. In contrast to expression of eNOS, iNOS protein level in the heart of DHT-treated rats was significantly elevated. Furthermore, cardiac protein level of alpha 1 subunit of the ATPase, as well as its plasma membrane content, were decreased in rats with PCOS. In line with this, alpha 2 subunit protein level in fraction of plasma membranes was also significantly below control level. In conclusion, DHT treatment impaired effectiveness of NOSs and Na+/K+-ATPase in the female rat heart. Regarding the importance of NO production and sodium/potassium transport in the cardiac contraction and blood flow regulation, it implicates strong consequences of PCOS for heart functioning.",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone",
volume = "123",
number = "5",
pages = "303-307",
doi = "10.1055/s-0035-1548929"
}
Tepavčević, S., Milutinovic, D. V., Macut, D., Stanišić, J., Nikolic, M., Bozic-Antic, I., Rodaljevic, S., Bjekic-Macut, J., Matić, G.,& Korićanac, G. (2015). Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone.
Experimental and Clinical Endocrinology and Diabetes, 123(5), 303-307.
https://doi.org/10.1055/s-0035-1548929
Tepavčević S, Milutinovic DV, Macut D, Stanišić J, Nikolic M, Bozic-Antic I, Rodaljevic S, Bjekic-Macut J, Matić G, Korićanac G. Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone. Experimental and Clinical Endocrinology and Diabetes. 2015;123(5):303-307
Tepavčević Snežana, Milutinovic D. V., Macut D., Stanišić Jelena, Nikolic M., Bozic-Antic I., Rodaljevic S., Bjekic-Macut J., Matić Gordana, Korićanac Goran, "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone" Experimental and Clinical Endocrinology and Diabetes, 123, no. 5 (2015):303-307,
https://doi.org/10.1055/s-0035-1548929 .
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GR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppression

Savić, Danka A.; Knežević, Goran; Damjanović, Svetozar S.; Antic, Jadranka; Matić, Gordana

(2014)

TY  - JOUR
AU  - Savić, Danka A.
AU  - Knežević, Goran
AU  - Damjanović, Svetozar S.
AU  - Antic, Jadranka
AU  - Matić, Gordana
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/108
AB  - Background: The hypothalamo-pituitary-adrenocortical (HPA) axis self-regulation is achieved via cortisol binding to mineralocorticoid (MR) and glucocorticoid receptors (GR). It is often disturbed in mental disorders, particularly in those where traumatic stress has been implicated, such as posttraumatic stress disorder and depression. Although dexamethasone suppression test (DST) is often used as diagnostic aid, the findings still vary. In search of the factors influencing the DST outcome, we examined the glucocorticoicl receptor (GR) gene Bell polymorphism. Methods: A total of 229 male subjects were classified into three Bell groups: two groups with homozygous carriers (of the G allele, N=108, and of the C allele, N=26), and one with heterozygous carriers (N=95). Multiple hierarchical linear regression analysis was clone, where the dependent variable was the clexamethasone-inclucecl cortisol suppression, and predictors included receptor variables. The interactions of the count of Gs with the predictors were introduced to single out the effects of the G allele. Results: The means of all studied variables, including suppression, are statistically the same in the three groups. However, the mechanism of suppression involves MRs only in the G allele carriers. Limitations: The subjects were selected by criteria suited for the aim of the large project whose part is this study, hence the relatively small number of CC carriers. Also, we did not assess MR functional properties that would probably sharpen the results. Conclusion: Our finding that MRs participate in cortisol suppression in the G allele carriers suggests that research aimed at refining HPA axis-based therapy might require its adjustment for such patients., (C) 2014 Elsevier By. All rights reserved.
T2  - Journal of Affective Disorders
T1  - GR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppression
VL  - 168
SP  - 1
EP  - 4
DO  - 10.1016/j.jad.2014.06.046
ER  - 
@article{
author = "Savić, Danka A. and Knežević, Goran and Damjanović, Svetozar S. and Antic, Jadranka and Matić, Gordana",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/108",
abstract = "Background: The hypothalamo-pituitary-adrenocortical (HPA) axis self-regulation is achieved via cortisol binding to mineralocorticoid (MR) and glucocorticoid receptors (GR). It is often disturbed in mental disorders, particularly in those where traumatic stress has been implicated, such as posttraumatic stress disorder and depression. Although dexamethasone suppression test (DST) is often used as diagnostic aid, the findings still vary. In search of the factors influencing the DST outcome, we examined the glucocorticoicl receptor (GR) gene Bell polymorphism. Methods: A total of 229 male subjects were classified into three Bell groups: two groups with homozygous carriers (of the G allele, N=108, and of the C allele, N=26), and one with heterozygous carriers (N=95). Multiple hierarchical linear regression analysis was clone, where the dependent variable was the clexamethasone-inclucecl cortisol suppression, and predictors included receptor variables. The interactions of the count of Gs with the predictors were introduced to single out the effects of the G allele. Results: The means of all studied variables, including suppression, are statistically the same in the three groups. However, the mechanism of suppression involves MRs only in the G allele carriers. Limitations: The subjects were selected by criteria suited for the aim of the large project whose part is this study, hence the relatively small number of CC carriers. Also, we did not assess MR functional properties that would probably sharpen the results. Conclusion: Our finding that MRs participate in cortisol suppression in the G allele carriers suggests that research aimed at refining HPA axis-based therapy might require its adjustment for such patients., (C) 2014 Elsevier By. All rights reserved.",
journal = "Journal of Affective Disorders",
title = "GR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppression",
volume = "168",
pages = "1-4",
doi = "10.1016/j.jad.2014.06.046"
}
Savić, D. A., Knežević, G., Damjanović, S. S., Antic, J.,& Matić, G. (2014). GR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppression.
Journal of Affective Disorders, 168, 1-4.
https://doi.org/10.1016/j.jad.2014.06.046
Savić DA, Knežević G, Damjanović SS, Antic J, Matić G. GR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppression. Journal of Affective Disorders. 2014;168:1-4
Savić Danka A., Knežević Goran, Damjanović Svetozar S., Antic Jadranka, Matić Gordana, "GR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppression" Journal of Affective Disorders, 168 (2014):1-4,
https://doi.org/10.1016/j.jad.2014.06.046 .
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Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD

Matić, Gordana; Milutinovic, Danijela Vojnovic; Nestorov, Jelena; Elakovic, Ivana; Jovanovic, Sanja Manitasevic; Elzaedi, Younis Mouftah; Perisic, Tatjana; Dunderski, Jadranka; Damjanović, Svetozar S.; Knežević, Goran; Spiric, Zeljko; Vermetten, Eric; Savić, Danka A.

(2014)

TY  - JOUR
AU  - Matić, Gordana
AU  - Milutinovic, Danijela Vojnovic
AU  - Nestorov, Jelena
AU  - Elakovic, Ivana
AU  - Jovanovic, Sanja Manitasevic
AU  - Elzaedi, Younis Mouftah
AU  - Perisic, Tatjana
AU  - Dunderski, Jadranka
AU  - Damjanović, Svetozar S.
AU  - Knežević, Goran
AU  - Spiric, Zeljko
AU  - Vermetten, Eric
AU  - Savić, Danka A.
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5909
AB  - Alterations in the number and functional status of mineralocorticoid (MR) and glucocorticoid receptors (GR) may contribute to vulnerability to posttraumatic stress disorder (PTSD). Corticosteroid receptors are chaperoned by heat shock proteins Hsp90 and Hsp70. We examined relations between corticosteroid receptor and heat shock protein expression levels, and related them with war trauma exposure, PTSD and resilience to PTSD. Relative levels of MR. Hsp90 and Hsp70 were determined by immunoblotting in lymphocytes from war trauma-exposed men with current PTSD (current PTSD group, n=113), with lifetime PTSD (life-time PTSD group, n=61) and without PTSD (trauma control group, n=88), and from non-traumatized healthy controls (healthy control group, n=85). Between-group differences in MR, Hsp90 and Hsp70 levels and in MR/GR ratio were not observed. The level of MR was correlated with both Hsp90 and Hsp70 levels in trauma control and healthy control groups. On the other hand, GR level was correlated only with Hsp90 level, and this correlation was evident in current PTSD and trauma control groups. In conclusion, PTSD and exposure to trauma are not related to changes in lymphocyte MR, Hsp90 or Hsp70 levels, but may be associated with disturbances in corticosteroid receptors interaction with heat shock proteins. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
T2  - Psychiatry Research
T1  - Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD
VL  - 215
IS  - 2
SP  - 379
EP  - 385
DO  - 10.1016/j.psychres.2013.11.022
ER  - 
@article{
author = "Matić, Gordana and Milutinovic, Danijela Vojnovic and Nestorov, Jelena and Elakovic, Ivana and Jovanovic, Sanja Manitasevic and Elzaedi, Younis Mouftah and Perisic, Tatjana and Dunderski, Jadranka and Damjanović, Svetozar S. and Knežević, Goran and Spiric, Zeljko and Vermetten, Eric and Savić, Danka A.",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5909",
abstract = "Alterations in the number and functional status of mineralocorticoid (MR) and glucocorticoid receptors (GR) may contribute to vulnerability to posttraumatic stress disorder (PTSD). Corticosteroid receptors are chaperoned by heat shock proteins Hsp90 and Hsp70. We examined relations between corticosteroid receptor and heat shock protein expression levels, and related them with war trauma exposure, PTSD and resilience to PTSD. Relative levels of MR. Hsp90 and Hsp70 were determined by immunoblotting in lymphocytes from war trauma-exposed men with current PTSD (current PTSD group, n=113), with lifetime PTSD (life-time PTSD group, n=61) and without PTSD (trauma control group, n=88), and from non-traumatized healthy controls (healthy control group, n=85). Between-group differences in MR, Hsp90 and Hsp70 levels and in MR/GR ratio were not observed. The level of MR was correlated with both Hsp90 and Hsp70 levels in trauma control and healthy control groups. On the other hand, GR level was correlated only with Hsp90 level, and this correlation was evident in current PTSD and trauma control groups. In conclusion, PTSD and exposure to trauma are not related to changes in lymphocyte MR, Hsp90 or Hsp70 levels, but may be associated with disturbances in corticosteroid receptors interaction with heat shock proteins. (C) 2013 Elsevier Ireland Ltd. All rights reserved.",
journal = "Psychiatry Research",
title = "Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD",
volume = "215",
number = "2",
pages = "379-385",
doi = "10.1016/j.psychres.2013.11.022"
}
Matić, G., Milutinovic, D. V., Nestorov, J., Elakovic, I., Jovanovic, S. M., Elzaedi, Y. M., Perisic, T., Dunderski, J., Damjanović, S. S., Knežević, G., Spiric, Z., Vermetten, E.,& Savić, D. A. (2014). Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD.
Psychiatry Research, 215(2), 379-385.
https://doi.org/10.1016/j.psychres.2013.11.022
Matić G, Milutinovic DV, Nestorov J, Elakovic I, Jovanovic SM, Elzaedi YM, Perisic T, Dunderski J, Damjanović SS, Knežević G, Spiric Z, Vermetten E, Savić DA. Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD. Psychiatry Research. 2014;215(2):379-385
Matić Gordana, Milutinovic Danijela Vojnovic, Nestorov Jelena, Elakovic Ivana, Jovanovic Sanja Manitasevic, Elzaedi Younis Mouftah, Perisic Tatjana, Dunderski Jadranka, Damjanović Svetozar S., Knežević Goran, Spiric Zeljko, Vermetten Eric, Savić Danka A., "Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD" Psychiatry Research, 215, no. 2 (2014):379-385,
https://doi.org/10.1016/j.psychres.2013.11.022 .
12
11
10

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

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

(2014)

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

Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD

Matić, Gordana; Milutinovic, Danijela Vojnovic; Nestorov, Jelena; Elakovic, Ivana; Jovanovic, Sanja Manitasevic; Perisic, Tatjana; Dunderski, Jadranka; Damjanović, Svetozar S.; Knežević, Goran; Spiric, Zeljko; Vermetten, Eric; Savić, Danka A.

(2013)

TY  - JOUR
AU  - Matić, Gordana
AU  - Milutinovic, Danijela Vojnovic
AU  - Nestorov, Jelena
AU  - Elakovic, Ivana
AU  - Jovanovic, Sanja Manitasevic
AU  - Perisic, Tatjana
AU  - Dunderski, Jadranka
AU  - Damjanović, Svetozar S.
AU  - Knežević, Goran
AU  - Spiric, Zeljko
AU  - Vermetten, Eric
AU  - Savić, Danka A.
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5429
AB  - Objective: Posttraumatic stress disorder (PTSD) has been shown to be associated with altered glucocorticoid receptor (GR) activity. We studied the expression and functional properties of the receptor in peripheral blood mononuclear cells (PBMCs) from non-traumatized healthy individuals (healthy controls; n = 85), and war trauma-exposed individuals with current PTSD (n = 113), with life-time PTSD (n = 61) and without PTSD (trauma controls; n = 88). The aim of the study was to distinguish the receptor alterations related to PTSD from those related to trauma itself or to resilience to PTSD. Methods: Functional status of the receptor was assessed by radioligand binding and lysozyme synthesis inhibition assays. The level of GR gene expression was measured by quantitative PCR and immunoblotting. Results: Current PTSD patients had the lowest, while trauma controls had the highest number of glucocorticoid binding sites (B-max) in PBMCs. Hormone-binding potential (B-max/K-D ratio) of the receptor was diminished in the current PTSD group in comparison to all other study groups. Correlation between B-max and K-D that normally exists in healthy individuals was decreased in the current PTSD group. Contrasting B-max data, GR protein level was lower in trauma controls than in participants with current or life-time PTSD. Conclusions: Current PTSD is characterized by reduced lymphocyte GR hormone-binding potential and by disturbed compensation between B-max and hormone-binding affinity. Resilience to PTSD is associated with enlarged fraction of the receptor molecules capable of hormone binding, within the total receptor molecule population in PBMCs. (C) 2013 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-psychopharmacology and Biological Psychiatry
T1  - Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD
VL  - 43
SP  - 238
EP  - 245
DO  - 10.1016/j.pnpbp.2013.01.005
ER  - 
@article{
author = "Matić, Gordana and Milutinovic, Danijela Vojnovic and Nestorov, Jelena and Elakovic, Ivana and Jovanovic, Sanja Manitasevic and Perisic, Tatjana and Dunderski, Jadranka and Damjanović, Svetozar S. and Knežević, Goran and Spiric, Zeljko and Vermetten, Eric and Savić, Danka A.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5429",
abstract = "Objective: Posttraumatic stress disorder (PTSD) has been shown to be associated with altered glucocorticoid receptor (GR) activity. We studied the expression and functional properties of the receptor in peripheral blood mononuclear cells (PBMCs) from non-traumatized healthy individuals (healthy controls; n = 85), and war trauma-exposed individuals with current PTSD (n = 113), with life-time PTSD (n = 61) and without PTSD (trauma controls; n = 88). The aim of the study was to distinguish the receptor alterations related to PTSD from those related to trauma itself or to resilience to PTSD. Methods: Functional status of the receptor was assessed by radioligand binding and lysozyme synthesis inhibition assays. The level of GR gene expression was measured by quantitative PCR and immunoblotting. Results: Current PTSD patients had the lowest, while trauma controls had the highest number of glucocorticoid binding sites (B-max) in PBMCs. Hormone-binding potential (B-max/K-D ratio) of the receptor was diminished in the current PTSD group in comparison to all other study groups. Correlation between B-max and K-D that normally exists in healthy individuals was decreased in the current PTSD group. Contrasting B-max data, GR protein level was lower in trauma controls than in participants with current or life-time PTSD. Conclusions: Current PTSD is characterized by reduced lymphocyte GR hormone-binding potential and by disturbed compensation between B-max and hormone-binding affinity. Resilience to PTSD is associated with enlarged fraction of the receptor molecules capable of hormone binding, within the total receptor molecule population in PBMCs. (C) 2013 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-psychopharmacology and Biological Psychiatry",
title = "Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD",
volume = "43",
pages = "238-245",
doi = "10.1016/j.pnpbp.2013.01.005"
}
Matić, G., Milutinovic, D. V., Nestorov, J., Elakovic, I., Jovanovic, S. M., Perisic, T., Dunderski, J., Damjanović, S. S., Knežević, G., Spiric, Z., Vermetten, E.,& Savić, D. A. (2013). Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD.
Progress in Neuro-psychopharmacology and Biological Psychiatry, 43, 238-245.
https://doi.org/10.1016/j.pnpbp.2013.01.005
Matić G, Milutinovic DV, Nestorov J, Elakovic I, Jovanovic SM, Perisic T, Dunderski J, Damjanović SS, Knežević G, Spiric Z, Vermetten E, Savić DA. Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD. Progress in Neuro-psychopharmacology and Biological Psychiatry. 2013;43:238-245
Matić Gordana, Milutinovic Danijela Vojnovic, Nestorov Jelena, Elakovic Ivana, Jovanovic Sanja Manitasevic, Perisic Tatjana, Dunderski Jadranka, Damjanović Svetozar S., Knežević Goran, Spiric Zeljko, Vermetten Eric, Savić Danka A., "Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD" Progress in Neuro-psychopharmacology and Biological Psychiatry, 43 (2013):238-245,
https://doi.org/10.1016/j.pnpbp.2013.01.005 .
35
33
29

Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism

Adžić, Miroslav; Lukić, Iva; Mitić, Miloš; Đorđević, Jelena D.; Elakovic, Ivana; Đorđević, Ana D.; Krstic-Demonacos, Marija; Matić, Gordana; Radoičić, Marija B.

(2013)

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Lukić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Elakovic, Ivana
AU  - Đorđević, Ana D.
AU  - Krstic-Demonacos, Marija
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2013
UR  - http://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 Elakovic, Ivana and Đorđević, Ana D. and Krstic-Demonacos, Marija and Matić, Gordana and Radoičić, Marija B.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5868",
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., Elakovic, I., Đorđević, A. D., Krstic-Demonacos, M., Matić, G.,& Radoičić, M. B. (2013). Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism.
Psychoneuroendocrinology, 38(12), 2914-2924.
https://doi.org/10.1016/j.psyneuen.2013.07.019
Adžić M, Lukić I, Mitić M, Đorđević JD, Elakovic I, Đorđević AD, Krstic-Demonacos M, Matić G, Radoičić MB. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. Psychoneuroendocrinology. 2013;38(12):2914-2924
Adžić Miroslav, Lukić Iva, Mitić Miloš, Đorđević Jelena D., Elakovic Ivana, Đorđević Ana D., Krstic-Demonacos Marija, Matić Gordana, Radoičić Marija B., "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism" Psychoneuroendocrinology, 38, no. 12 (2013):2914-2924,
https://doi.org/10.1016/j.psyneuen.2013.07.019 .
28
26
26

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

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

(2013)

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

The role of personality and traumatic events in cortisol levels - Where does PTSD fit in?

Savić, Danka A.; Knežević, Goran; Damjanović, Svetozar S.; Spiric, Zeljko; Matić, Gordana

(2012)

TY  - JOUR
AU  - Savić, Danka A.
AU  - Knežević, Goran
AU  - Damjanović, Svetozar S.
AU  - Spiric, Zeljko
AU  - Matić, Gordana
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4879
AB  - Background: Studies of cortisol in post-traumatic stress disorder (PTSD) have yielded mixed results. We hypothesize that personality traits and traumatic experiences could be the confounders of cortisol measures and disease symptoms. Method: This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions on 400 male participants categorized by four groups: (A) 133 with current PTSD, (B) 66 with lifetime PTSD, (C) 102 trauma controls, and (D) 99 healthy controls (matched by age and education). Cortisol and ACTH were measured in blood samples taken hourly from 22:00 h to 09:00 h, with an additional sample at 07:30 h (resting state and morning rise). The next night, dexamethasone (0.5 mg) suppression test was performed. Results: No significant differences in basal cortisol and ACTH were found between study groups. The trait Conscientiousness, negatively modulated by Extraversion (assessed by NEO Personality Inventory-Revised) was found to correlate with cortisol (but not with ACTH). Group differences are found on suppression. Structural equation modeling shows excellent fit only when the paths (influences) from Conscientiousness to basal cortisol and from traumatic events to suppression are present. The paths connecting suppression and PTSD symptoms do not contribute. Conclusions: Two sources of differences of hypothalamo-pituitary-adrenocortical axis functioning are implied, both only indirectly connected to PTSD. It seems that basal cortisol secretion is associated more tightly with personality (introvertively modulated Conscientiousness), while the regulation by glucocorticoid receptor system is sensitized by repeated traumatic situations. (c) 2011 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - The role of personality and traumatic events in cortisol levels - Where does PTSD fit in?
VL  - 37
IS  - 7
SP  - 937
EP  - 947
DO  - 10.1016/j.psyneuen.2011.11.001
ER  - 
@article{
author = "Savić, Danka A. and Knežević, Goran and Damjanović, Svetozar S. and Spiric, Zeljko and Matić, Gordana",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4879",
abstract = "Background: Studies of cortisol in post-traumatic stress disorder (PTSD) have yielded mixed results. We hypothesize that personality traits and traumatic experiences could be the confounders of cortisol measures and disease symptoms. Method: This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions on 400 male participants categorized by four groups: (A) 133 with current PTSD, (B) 66 with lifetime PTSD, (C) 102 trauma controls, and (D) 99 healthy controls (matched by age and education). Cortisol and ACTH were measured in blood samples taken hourly from 22:00 h to 09:00 h, with an additional sample at 07:30 h (resting state and morning rise). The next night, dexamethasone (0.5 mg) suppression test was performed. Results: No significant differences in basal cortisol and ACTH were found between study groups. The trait Conscientiousness, negatively modulated by Extraversion (assessed by NEO Personality Inventory-Revised) was found to correlate with cortisol (but not with ACTH). Group differences are found on suppression. Structural equation modeling shows excellent fit only when the paths (influences) from Conscientiousness to basal cortisol and from traumatic events to suppression are present. The paths connecting suppression and PTSD symptoms do not contribute. Conclusions: Two sources of differences of hypothalamo-pituitary-adrenocortical axis functioning are implied, both only indirectly connected to PTSD. It seems that basal cortisol secretion is associated more tightly with personality (introvertively modulated Conscientiousness), while the regulation by glucocorticoid receptor system is sensitized by repeated traumatic situations. (c) 2011 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "The role of personality and traumatic events in cortisol levels - Where does PTSD fit in?",
volume = "37",
number = "7",
pages = "937-947",
doi = "10.1016/j.psyneuen.2011.11.001"
}
Savić, D. A., Knežević, G., Damjanović, S. S., Spiric, Z.,& Matić, G. (2012). The role of personality and traumatic events in cortisol levels - Where does PTSD fit in?.
Psychoneuroendocrinology, 37(7), 937-947.
https://doi.org/10.1016/j.psyneuen.2011.11.001
Savić DA, Knežević G, Damjanović SS, Spiric Z, Matić G. The role of personality and traumatic events in cortisol levels - Where does PTSD fit in?. Psychoneuroendocrinology. 2012;37(7):937-947
Savić Danka A., Knežević Goran, Damjanović Svetozar S., Spiric Zeljko, Matić Gordana, "The role of personality and traumatic events in cortisol levels - Where does PTSD fit in?" Psychoneuroendocrinology, 37, no. 7 (2012):937-947,
https://doi.org/10.1016/j.psyneuen.2011.11.001 .
1
19
16
18

Is there a biological difference between trauma-related depression and PTSD? DST says NO

Savić, Danka A.; Knežević, Goran; Damjanović, Svetozar S.; Spiric, Zeljko; Matić, Gordana

(2012)

TY  - JOUR
AU  - Savić, Danka A.
AU  - Knežević, Goran
AU  - Damjanović, Svetozar S.
AU  - Spiric, Zeljko
AU  - Matić, Gordana
PY  - 2012
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/4997
AB  - The use of the low-dose dexamethasone suppression test (DST) as a potentially discriminative marker between post-traumatic stress disorder (PTSD) and depression is still under discussion. In order to compare the influence of these psychopathologies on the DST results, we examined suppression in war-traumatized subjects with one or both of these disorders, as well as in healthy controls. Based on our previous findings, we hypothesized that subjects with any disorder would exhibit higher dexamethasone suppression than healthy controls due to traumatic experiences. This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions on 399 mate participants: 57 with PTSD, 28 with depression, 76 with PTSD + depression, and 238 healthy controls. Cortisol was measured in blood samples taken at 0900 h before and after administering 0.5 mg of dexamethasone (at 2300 h). Group means standard deviation of cortisol suppression were: 79.4 +/- 18.5 in the PTSD group, 80.8 +/- 11.6 in the depression group, 77.5 +/- 24.6 in the group with PTSD+depression, and 66.8 +/- 34.6 in healthy controls. The first three groups suppressed significantly more than the fourth. When the number of traumas was introduced as a covariate, the differences disappeared. The hypothesis was confirmed: in respect to DST, the examined trauma-related psychopathologies showed the same pattern: hypersuppression, due to multiple traumatic experiences. (C) 2012 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - Is there a biological difference between trauma-related depression and PTSD? DST says NO
VL  - 37
IS  - 9
SP  - 1516
EP  - 1520
DO  - 10.1016/j.psyneuen.2012.02.005
ER  - 
@article{
author = "Savić, Danka A. and Knežević, Goran and Damjanović, Svetozar S. and Spiric, Zeljko and Matić, Gordana",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4997",
abstract = "The use of the low-dose dexamethasone suppression test (DST) as a potentially discriminative marker between post-traumatic stress disorder (PTSD) and depression is still under discussion. In order to compare the influence of these psychopathologies on the DST results, we examined suppression in war-traumatized subjects with one or both of these disorders, as well as in healthy controls. Based on our previous findings, we hypothesized that subjects with any disorder would exhibit higher dexamethasone suppression than healthy controls due to traumatic experiences. This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions on 399 mate participants: 57 with PTSD, 28 with depression, 76 with PTSD + depression, and 238 healthy controls. Cortisol was measured in blood samples taken at 0900 h before and after administering 0.5 mg of dexamethasone (at 2300 h). Group means standard deviation of cortisol suppression were: 79.4 +/- 18.5 in the PTSD group, 80.8 +/- 11.6 in the depression group, 77.5 +/- 24.6 in the group with PTSD+depression, and 66.8 +/- 34.6 in healthy controls. The first three groups suppressed significantly more than the fourth. When the number of traumas was introduced as a covariate, the differences disappeared. The hypothesis was confirmed: in respect to DST, the examined trauma-related psychopathologies showed the same pattern: hypersuppression, due to multiple traumatic experiences. (C) 2012 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "Is there a biological difference between trauma-related depression and PTSD? DST says NO",
volume = "37",
number = "9",
pages = "1516-1520",
doi = "10.1016/j.psyneuen.2012.02.005"
}
Savić, D. A., Knežević, G., Damjanović, S. S., Spiric, Z.,& Matić, G. (2012). Is there a biological difference between trauma-related depression and PTSD? DST says NO.
Psychoneuroendocrinology, 37(9), 1516-1520.
https://doi.org/10.1016/j.psyneuen.2012.02.005
Savić DA, Knežević G, Damjanović SS, Spiric Z, Matić G. Is there a biological difference between trauma-related depression and PTSD? DST says NO. Psychoneuroendocrinology. 2012;37(9):1516-1520
Savić Danka A., Knežević Goran, Damjanović Svetozar S., Spiric Zeljko, Matić Gordana, "Is there a biological difference between trauma-related depression and PTSD? DST says NO" Psychoneuroendocrinology, 37, no. 9 (2012):1516-1520,
https://doi.org/10.1016/j.psyneuen.2012.02.005 .
1
13
13
13

Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats

Đorđević, Ana D.; Đorđević, Jelena D.; Elakovic, Ivana; Adžić, Miroslav; Matić, Gordana; Radoičić, Marija B.

(2012)

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elakovic, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2012
UR  - http://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 Elakovic, Ivana and Adžić, Miroslav and Matić, Gordana and Radoičić, Marija B.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4678",
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., Elakovic, I., Adžić, M., Matić, G.,& Radoičić, M. B. (2012). Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats.
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, Elakovic I, Adžić M, Matić G, Radoičić MB. Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. Progress in Neuro-psychopharmacology and Biological Psychiatry. 2012;36(1):92-100
Đorđević Ana D., Đorđević Jelena D., Elakovic Ivana, Adžić Miroslav, Matić Gordana, Radoičić Marija B., "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats" Progress in Neuro-psychopharmacology and Biological Psychiatry, 36, no. 1 (2012):92-100,
https://doi.org/10.1016/j.pnpbp.2011.10.006 .
41
38
39

Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex

Đorđević, Ana D.; Đorđević, Jelena D.; Elakovic, Ivana; Adžić, Miroslav; Matić, Gordana; Radoičić, Marija B.

(2012)

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elakovic, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2012
UR  - http://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 Elakovic, Ivana and Adžić, Miroslav and Matić, Gordana and Radoičić, Marija B.",
year = "2012",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5042",
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., Elakovic, I., Adžić, M., Matić, G.,& Radoičić, M. B. (2012). Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex.
European Journal of Pharmacology, 693(1-3), 37-44.
https://doi.org/10.1016/j.ejphar.2012.07.042
Đorđević AD, Đorđević JD, Elakovic I, Adžić M, Matić G, Radoičić MB. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. European Journal of Pharmacology. 2012;693(1-3):37-44
Đorđević Ana D., Đorđević Jelena D., Elakovic Ivana, Adžić Miroslav, Matić Gordana, Radoičić Marija B., "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex" European Journal of Pharmacology, 693, no. 1-3 (2012):37-44,
https://doi.org/10.1016/j.ejphar.2012.07.042 .
17
18
19

Gender-specific response of brain corticosteroid receptors to stress and fluoxetine

Elakovic, Ivana; Đorđević, Ana D.; Adžić, Miroslav; Đorđević, Jelena D.; Radoičić, Marija B.; Matić, Gordana

(2011)

TY  - JOUR
AU  - Elakovic, Ivana
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radoičić, Marija B.
AU  - Matić, Gordana
PY  - 2011
UR  - http://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 = "Elakovic, Ivana and Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radoičić, Marija B. and Matić, Gordana",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4277",
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"
}
Elakovic, I., Đorđević, A. D., Adžić, M., Đorđević, J. D., Radoičić, M. B.,& Matić, G. (2011). Gender-specific response of brain corticosteroid receptors to stress and fluoxetine.
Brain Research, 1384, 61-68.
https://doi.org/10.1016/j.brainres.2011.01.078
Elakovic I, Đorđević AD, Adžić M, Đorđević JD, Radoičić MB, Matić G. Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. Brain Research. 2011;1384:61-68
Elakovic Ivana, Đorđević Ana D., Adžić Miroslav, Đorđević Jelena D., Radoičić Marija B., Matić Gordana, "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine" Brain Research, 1384 (2011):61-68,
https://doi.org/10.1016/j.brainres.2011.01.078 .
17
16
16

Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver

Đorđević, Jelena D.; Đorđević, Ana D.; Adžić, Miroslav; Elakovic, Ivana; Matić, Gordana; Radoičić, Marija B.

(2011)

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Elakovic, Ivana
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2011
UR  - http://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 Elakovic, Ivana and Matić, Gordana and Radoičić, Marija B.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4329",
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., Elakovic, I., Matić, G.,& Radoičić, M. B. (2011). Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver.
European Journal of Pharmacology, 659(1), 61-66.
https://doi.org/10.1016/j.ejphar.2011.03.003
Đorđević JD, Đorđević AD, Adžić M, Elakovic I, Matić G, Radoičić MB. Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. European Journal of Pharmacology. 2011;659(1):61-66
Đorđević Jelena D., Đorđević Ana D., Adžić Miroslav, Elakovic Ivana, Matić Gordana, Radoičić Marija B., "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver" European Journal of Pharmacology, 659, no. 1 (2011):61-66,
https://doi.org/10.1016/j.ejphar.2011.03.003 .
46
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Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats

Adžić, Miroslav; Đorđević, Jelena D.; Mitić, Miloš; Simić, Iva; Rackov, Gorjana; Đorđević, Ana D.; Elakovic, Ivana; Matić, Gordana; Radoičić, Marija B.

(2011)

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Rackov, Gorjana
AU  - Đorđević, Ana D.
AU  - Elakovic, Ivana
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2011
UR  - http://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
ER  - 
@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Mitić, Miloš and Simić, Iva and Rackov, Gorjana and Đorđević, Ana D. and Elakovic, Ivana and Matić, Gordana and Radoičić, Marija B.",
year = "2011",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/4640",
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"
}
Adžić, M., Đorđević, J. D., Mitić, M., Simić, I., Rackov, G., Đorđević, A. D., Elakovic, I., Matić, G.,& Radoičić, M. B. (2011). Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats.
Acta Chimica Slovenica, 58(4), 785-791.
Adžić M, Đorđević JD, Mitić M, Simić I, Rackov G, Đorđević AD, Elakovic I, Matić G, Radoičić MB. Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. Acta Chimica Slovenica. 2011;58(4):785-791
Adžić Miroslav, Đorđević Jelena D., Mitić Miloš, Simić Iva, Rackov Gorjana, Đorđević Ana D., Elakovic Ivana, Matić Gordana, Radoičić Marija B., "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats" Acta Chimica Slovenica, 58, no. 4 (2011):785-791
4

Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine

Elakovic, Ivana; Vasiljevic, Dorde; Adžić, Miroslav; Đorđević, Ana D.; Đorđević, Jelena D.; Radoičić, Marija B.; Matić, Gordana

(2010)

TY  - JOUR
AU  - Elakovic, Ivana
AU  - Vasiljevic, Dorde
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Radoičić, Marija B.
AU  - Matić, Gordana
PY  - 2010
UR  - http://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 = "Elakovic, Ivana and Vasiljevic, Dorde and Adžić, Miroslav and Đorđević, Ana D. and Đorđević, Jelena D. and Radoičić, Marija B. and Matić, Gordana",
year = "2010",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3960",
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"
}
Elakovic, I., Vasiljevic, D., Adžić, M., Đorđević, A. D., Đorđević, J. D., Radoičić, M. B.,& Matić, G. (2010). Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine.
European Journal of Pharmacology, 632(1-3), 79-85.
https://doi.org/10.1016/j.ejphar.2010.01.015
Elakovic I, Vasiljevic D, Adžić M, Đorđević AD, Đorđević JD, Radoičić MB, Matić G. Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine. European Journal of Pharmacology. 2010;632(1-3):79-85
Elakovic Ivana, Vasiljevic Dorde, Adžić Miroslav, Đorđević Ana D., Đorđević Jelena D., Radoičić Marija B., Matić Gordana, "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine" European Journal of Pharmacology, 632, no. 1-3 (2010):79-85,
https://doi.org/10.1016/j.ejphar.2010.01.015 .
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Radiation-induced hyposuppression of the hypothalamic-pituitary-adrenal axis is associated with alterations of hippocampal corticosteroid receptor expression

Velickovic, Natasa; Đorđević, Ana D.; Matić, Gordana; Horvat, Anica

(2008)

TY  - JOUR
AU  - Velickovic, Natasa
AU  - Đorđević, Ana D.
AU  - Matić, Gordana
AU  - Horvat, Anica
PY  - 2008
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/3395
AB  - Therapeutic brain irradiation in children can cause a progressive decline in cognitive functions through a diminished capability to learn and memorize. Because of the known involvement of the hippocampus in memory consolidation, this study was aimed at examining the late effects of y radiation on hypothalamic-pituitary-adrenal (HPA) axis activity and hippocampal corticosteroid receptor expression in an animal model of cranial radiotherapy. In the late-response phase, the basal and stress-induced corticosterone levels were not affected by radiation, but the suppression of glucocorticoid negative feedback by dexamethasone was attenuated in irradiated rats. Western blot analyses showed that exposure to radiation led to a decrease of cytosolic glucocorticoid receptor (GR) levels and a concomitant elevation of mineralocorticoid receptor (MR). The results obtained were complemented by those of RT-PCR, since the ratio of GR/MR mRNA was also decreased after radiation exposure. Dexamethasone appeared to be much less effective in shifting GR to the nuclear compartment in irradiated rats than in sham-irradiated animals. However, the expression of chaperones that aid GR intracellular trafficking, Hsp90 and Hsp70, remained unaffected. In conclusion, our data suggest that the hallmark of the late response to y radiation is a hyposuppressive state of the HPA axis that is associated with a decrease in both the GR/MR ratio and the nuclear accumulation of dexamethasone-activated GR in the hippocampus. (c) 2008 by Radiation Research Society.
T2  - Radiation Research
T1  - Radiation-induced hyposuppression of the hypothalamic-pituitary-adrenal axis is associated with alterations of hippocampal corticosteroid receptor expression
VL  - 169
IS  - 4
SP  - 397
EP  - 407
DO  - 10.1667/RR1200.1
ER  - 
@article{
author = "Velickovic, Natasa and Đorđević, Ana D. and Matić, Gordana and Horvat, Anica",
year = "2008",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/3395",
abstract = "Therapeutic brain irradiation in children can cause a progressive decline in cognitive functions through a diminished capability to learn and memorize. Because of the known involvement of the hippocampus in memory consolidation, this study was aimed at examining the late effects of y radiation on hypothalamic-pituitary-adrenal (HPA) axis activity and hippocampal corticosteroid receptor expression in an animal model of cranial radiotherapy. In the late-response phase, the basal and stress-induced corticosterone levels were not affected by radiation, but the suppression of glucocorticoid negative feedback by dexamethasone was attenuated in irradiated rats. Western blot analyses showed that exposure to radiation led to a decrease of cytosolic glucocorticoid receptor (GR) levels and a concomitant elevation of mineralocorticoid receptor (MR). The results obtained were complemented by those of RT-PCR, since the ratio of GR/MR mRNA was also decreased after radiation exposure. Dexamethasone appeared to be much less effective in shifting GR to the nuclear compartment in irradiated rats than in sham-irradiated animals. However, the expression of chaperones that aid GR intracellular trafficking, Hsp90 and Hsp70, remained unaffected. In conclusion, our data suggest that the hallmark of the late response to y radiation is a hyposuppressive state of the HPA axis that is associated with a decrease in both the GR/MR ratio and the nuclear accumulation of dexamethasone-activated GR in the hippocampus. (c) 2008 by Radiation Research Society.",
journal = "Radiation Research",
title = "Radiation-induced hyposuppression of the hypothalamic-pituitary-adrenal axis is associated with alterations of hippocampal corticosteroid receptor expression",
volume = "169",
number = "4",
pages = "397-407",
doi = "10.1667/RR1200.1"
}
Velickovic, N., Đorđević, A. D., Matić, G.,& Horvat, A. (2008). Radiation-induced hyposuppression of the hypothalamic-pituitary-adrenal axis is associated with alterations of hippocampal corticosteroid receptor expression.
Radiation Research, 169(4), 397-407.
https://doi.org/10.1667/RR1200.1
Velickovic N, Đorđević AD, Matić G, Horvat A. Radiation-induced hyposuppression of the hypothalamic-pituitary-adrenal axis is associated with alterations of hippocampal corticosteroid receptor expression. Radiation Research. 2008;169(4):397-407
Velickovic Natasa, Đorđević Ana D., Matić Gordana, Horvat Anica, "Radiation-induced hyposuppression of the hypothalamic-pituitary-adrenal axis is associated with alterations of hippocampal corticosteroid receptor expression" Radiation Research, 169, no. 4 (2008):397-407,
https://doi.org/10.1667/RR1200.1 .
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