TY  - JOUR
AU  - Tepavcevic, S.
AU  - Vojnović-Milutinović, Danijela
AU  - Macut, D.
AU  - Stanisic, J.
AU  - Nikolic, M.
AU  - Bozic-Antic, I.
AU  - Rodaljevic, S.
AU  - Bjekić-Macut, Jelica
AU  - Matić, Gordana
AU  - Koricanac, G.
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1961
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 & Diabetes
T1  - Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of
 Polycystic Ovary Syndrome Induced by Dihydrotestosterone
IS  - 5
VL  - 123
DO  - 10.1055/s-0035-1548929
SP  - 303
EP  - 307
ER  - 

@article{
author = "Tepavcevic, S. and Vojnović-Milutinović, Danijela and Macut, D. and Stanisic, J. and Nikolic, M. and Bozic-Antic, I. and Rodaljevic, S. and Bjekić-Macut, Jelica and Matić, Gordana and Koricanac, G.",
year = "2015",
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 & Diabetes",
title = "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of
 Polycystic Ovary Syndrome Induced by Dihydrotestosterone",
number = "5",
volume = "123",
doi = "10.1055/s-0035-1548929",
pages = "303-307"
}

Tepavcevic, S., Vojnović-Milutinović, D., Macut, D., Stanisic, J., Nikolic, M., Bozic-Antic, I., Rodaljevic, S., Bjekić-Macut, J., Matić, G.,& Koricanac, G.. (2015). Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of
 Polycystic Ovary Syndrome Induced by Dihydrotestosterone. in Experimental and Clinical Endocrinology & Diabetes, 123(5), 303-307.
https://doi.org/10.1055/s-0035-1548929

Tepavcevic S, Vojnović-Milutinović D, Macut D, Stanisic J, Nikolic M, Bozic-Antic I, Rodaljevic S, Bjekić-Macut J, Matić G, Koricanac G. Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of
 Polycystic Ovary Syndrome Induced by Dihydrotestosterone. in Experimental and Clinical Endocrinology & Diabetes. 2015;123(5):303-307.
doi:10.1055/s-0035-1548929 .

Tepavcevic, S., Vojnović-Milutinović, Danijela, Macut, D., Stanisic, J., Nikolic, M., Bozic-Antic, I., Rodaljevic, S., Bjekić-Macut, Jelica, Matić, Gordana, Koricanac, G., "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of
 Polycystic Ovary Syndrome Induced by Dihydrotestosterone" in Experimental and Clinical Endocrinology & Diabetes, 123, no. 5 (2015):303-307,
https://doi.org/10.1055/s-0035-1548929 . .