![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
| Item Type: | Article |
|---|---|
| Title: | Genetic deletion of the Angiotensin-(1-7) receptor Mas leads a reduced ovulatory rate |
| Creators Name: | Honorato-Sampaio, K., Ferreira Andrade, R., Bader, M., de Souza Martins, A., 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
