miR-181a promotes porcine granulosa cell apoptosis by targeting TGFBR1 via the activin signaling pathway

Publication date: Available online 28 September 2019Source: Molecular and Cellular EndocrinologyAuthor(s): Jia-Qing Zhang, Bin-Wen Gao, Hong-Xia Guo, Qiao-Ling Ren, Xian-Wei Wang, Jun-Feng Chen, Jing Wang, Zi-Jing Zhang, Qiang Ma, Bao-Song XingAbstractActivin/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-β 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-β 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.

Source: Molecular and Cellular Endocrinology - September 29, 2019 Category: Endocrinology Source Type: research