| First Author | Xiong F | Year | 2016 |
| Journal | Biol Open | Volume | 5 |
| Issue | 3 | Pages | 367-71 |
| PubMed ID | 26912776 | Mgi Jnum | J:231515 |
| Mgi Id | MGI:5771705 | Doi | 10.1242/bio.016907 |
| Citation | Xiong F, et al. (2016) miR-22 inhibits mouse ovarian granulosa cell apoptosis by targeting SIRT1. Biol Open 5(3):367-71 |
| abstractText | Granulosa cell (GC) apoptosis has been shown to be involved in follicular atresia, which is a degenerative process in ovarian follicles of mammals. However, the mechanism underlying the regulation of follicular atresia, particularly by microRNAs, is not well known. Real-time PCR (RT-PCR) was used to detect the expression level of miR-22 in healthy follicles (HF), early atretic follicles (EAF), and progressively atretic follicles (PAF). Flow cytometry was performed to assess the apoptosis of mouse granulosa cells (mGCs) treated with miR-22 mimics or negative control (NC) mimics. Regulation of the expression of SIRT1 by miR-22 was evaluated using a luciferase reporter assay system. To investigate the roles of SIRT1 in mGC apoptosis, the endogenous SIRT1 gene in mGCs was knocked down using an siRNA specific for SIRT1. miR-22 was increased during follicular atresia and suppressed granulosa cell apoptosis. The results of the luciferase reporter assay indicated that SIRT1 was a target gene of miR-22. In addition, knockdown of SIRT1 attenuated apoptosis in mGCs. miR-22 inhibits mGC apoptosis by downregulating SIRT1 directly in vitro. This study provides important insights into understanding the regulation mechanism of ovarian follicle atresia. |
