miR-181a promotes porcine granulosa cell apoptosis by targeting TGFBR1 via the activin signaling pathway
文献类型： 外文期刊
第一作者： Zhang, Jia-Qing
作者： Zhang, Jia-Qing;Gao, Bin-Wen;Guo, Hong-Xia;Ren, Qiao-Ling;Chen, Jun-Feng;Wang, Jing;Zhang, Zi-Jing;Ma, Qiang;Xing, Bao-Song;Zhang, Jia-Qing;Gao, Bin-Wen;Guo, Hong-Xia;Ren, Qiao-Ling;Chen, Jun-Feng;Wang, Jing;Zhang, Zi-Jing;Ma, Qiang;Xing, Bao-Song;Wang, Xian-Wei
作者机构：
关键词： miR-181a; Porcine granulosa cell; Apoptosis; TGFBR1; TGF-beta signaling
期刊名称：MOLECULAR AND CELLULAR ENDOCRINOLOGY （ 影响因子：4.102； 五年影响因子：4.226 ）
ISSN： 0303-7207
年卷期： 2020 年 499 卷
页码：
收录情况： SCI
摘要： Activin/Smad3 signaling plays a pivotal role in follicle development and atresia. However, the precise mechanisms underlying this process are not yet fully understood. Herein, we identified miR-181a as a central component of activin/Smad3-mediated follicle atresia. miR-181a was strikingly upregulated in porcine atretic follicles, which induced the apoptosis of porcine granulosa cells (GCs) in vitro. Furthermore, the transforming growth factor-beta type 1 receptor (TGFBR1) was confirmed as a direct target of miR-181a by bioinformatics analysis and luciferase assays. Transfection with an miR-181a agomir repressed the TGFBR1 mRNA and protein levels. In addition, TGFBR1 overexpression repressed GC apoptosis, whereas TGFBR1 inhibition promoted GC apoptosis. miR-181a overexpression downregulated the phosphorylation of Smad3 and blocked the activation of TGF-beta signaling. Moreover, activin A downregulated miR-181a expression and upregulated the TGFBR1 and p-Smad3 protein levels. Collectively, these data suggest that miR-181a regulates porcine GC apoptosis by targeting TGFBR1 via the activin signaling pathway.
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