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Angiotensin-(1-7), Angiotensin-Converting Enzyme 2 and Mas Receptor in Rat Polycystic Ovaries. | LitMetric

Angiotensin-(1-7), Angiotensin-Converting Enzyme 2 and Mas Receptor in Rat Polycystic Ovaries.

Protein Pept Lett

Department of Physiology and Biophysics, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

Published: July 2021

AI Article Synopsis

  • - Hyperandrogenism is linked to polycystic ovary syndrome (PCOS), but the role of the Ang-(1-7) peptide from the renin-angiotensin system in androgen excess is not completely understood.
  • - In a rat model mimicking PCOS, researchers found lower levels of Ang-(1-7) and its receptor Mas, as well as reduced expression of the enzyme ACE2, compared to normal ovaries.
  • - The study concluded that the ACE2-Ang-(1-7)-Mas receptor pathway is likely inhibited in polycystic ovaries, suggesting it may not contribute to the elevated testosterone levels associated with PCOS.

Article Abstract

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.

Download full-text PDF

Source
http://dx.doi.org/10.2174/0929866527666200826104410DOI Listing

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