Genetic deletion of the Angiotensin-(1-7) receptor Mas leads a reduced ovulatory rate

Item Type:	Article
Title:	Genetic deletion of the Angiotensin-(1-7) receptor Mas leads a reduced ovulatory rate
Creators Name:	Honorato-Sampaio, K. and Ferreira Andrade, R. and Bader, M. and de Souza Martins, A. and Souza Santos, R.A. and Reis, A.M.
Abstract:	Angiotensin-(1-7) [Ang-(1-7)] is a component of Renin-Angiotensin System (RAS) that acts through activation of the G-protein-coupled receptor Mas. Recent studies highlight Ang-(1-7) as an intermediate of gonadotropin in ovarian physiology. Genetically Mas-deficient mice allow the investigation of Ang-(1-7) in the ovulatory process. Therefore, the present study aimed to analyze the effects of Mas gene deletion on ovulation to confirm our hypothesis that Mas Knockout (Mas-KO) mice exhibit impairment in the ovulatory outcome. First, we evaluated the breeding data from our animal facilities and from a breeding experiment. The ovulation was observed directly from oviducts after a superovulation protocol and in the estrus morning. We also checked the follicular pool and mRNA expression of Insulin-like growth factor-1 (IGF-1) in ovaries to investigate a possible reason underlying the reduced ovulation. Mas-KO mice showed a reduced litter size and decreased spontaneous ovulatory rate. Ovarian stimulation by gonadotropins reversed ovulation outcome in Mas-KO mice. Mas deficiency also promoted a reduced ovarian follicular pool and lower IGF-1 mRNA levels, suggesting that Mas receptor plays a role in the survival of ovarian follicle. The reduction of ovulatory rate highlights the relevance of Ang-(1-7)/Mas axis in female reproduction, probably through a reduction of IGF-1 mRNA levels.
Keywords:	Mas Receptor, Knockout, Ovulation, Follicular Pool, IGF-1, Animals, Mice
Source:	Peptides
ISSN:	0196-9781
Publisher:	Elsevier
Volume:	107
Page Range:	83-88
Date:	September 2018
Official Publication:	https://doi.org/10.1016/j.peptides.2018.08.007
PubMed:	View item in PubMed

Repository Staff Only: item control page