Journal
PROTEIN AND PEPTIDE LETTERS
Volume 28, Issue 3, Pages 249-254Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/0929866527666200826104410
Keywords
Angiotensin-(1-7); mas receptor; ovary; steroidogenesis; PCOs; renin-angiotensin system
Categories
Funding
- FAPEMIG
- CAPES
- CNPq [04/2011-PPP]
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The study found that levels of Ang-(1-7) and Mas receptor were reduced in PCO compared to normal ovaries, and ACE2 mRNA expression was decreased in PCO as well. This suggests that the ovarian ACE2-Ang-(1-7)-Mas receptor axis is inhibited in rat PCO and may not be a co-factor of excess testosterone production.
Background: Hyperandrogenism is a pivotal mediator in the pathogenesis of the polycystic ovary syndrome (PCOS), but the mechanisms of androgen excess in this condition are not fully understood. Angiotensin (Ang)-(1-7) is an active peptide of the renin-angiotensin system (RAS) that stimulates ovarian follicular growth and testosterone release in vitro. Objective: To investigate whether Ang-(1-7), its receptor Mas and angiotensin-converting enzyme 2 (ACE2), the enzyme that converts Ang II into Ang-(1-7), are expressed in rat polycystic ovaries (PCO) and thus if this peptide system might be associated with excess androgen production in PCO. Methods: A rat model that shares some features of PCOS such as disruption of folliculogenesis and multiple ovarian cyst formation was used in the study. Results: We found reduced levels of Ang-(1-7) and Mas receptor in PCO compared to normal ovaries. Also, ACE2 mRNA expression was reduced in PCO compared to ovaries of control rats (p < 0.05). PCO had high levels of estrogen and testosterone and increased mRNA for upstream enzymes of the steroidogenic cascade, but not of P450 aromatase. Conclusion: These findings suggest that the ovarian ACE2-Ang-(1-7)-Mas receptor axis is inhibited and therefore may not be a co-factor of excess testosterone production in rat PCO.
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