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

MOLECULAR AND CELLULAR ENDOCRINOLOGY

卷:499

Article

Zhang, Jia-Qing^1,2  Gao, Bin-Wen^1,2  Guo, Hong-Xia^1,2  Ren, Qiao-Ling^1,2  Wang, Xian-Wei³  Chen, Jun-Feng^1,2  Wang, Jing^1,2  Zhang, Zi-Jing^1,2  Ma, Qiang^1,2  Xing, Bao-Song^1,2 

[1] Henan Acad Agr Sci, Inst Anim Husb & Vet Sci, Zhengzhou 450002, Henan, Peoples R China

[2] Henan Key Lab Farm Anim Breeding & Nutr Regulat, Zhengzhou 450002, Henan, Peoples R China

[3] Henan Prov Anim Husb Gen Stn, Zhengzhou 450008, Henan, Peoples R China

关键词: miR-181a;    Porcine granulosa cell;    Apoptosis;    TGFBR1;    TGF-beta signaling;   

DOI  :  10.1016/j.mce.2019.110603

来源: Elsevier

【 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.

【 授权许可】

Free