Vigilin interacts with ER-β to protect against palmitic acid-induced granulosa cells apoptosis via inhibiting calcineurin-mediated Drp1 signaling pathway

Vigilin 与 ER-β 相互作用通过抑制钙调神经磷酸酶介导的 Drp1 信号通路防止棕榈酸诱导的颗粒细胞凋亡

阅读:4
作者:Hong-Qing Liao, Jun Zhou, Yang Cao, Yu-Lin Nie, Mei-Qing Li, Jing Zhou

Background

Hypercholesterolemia is one of the causes of female infertility, and as a common fatty acid in follicular fluid, palmitic acid (PA) level plays a vital role in granule cell which is closely related to the developmental potential of follicle.

Conclusion

Vigilin could interact with ER-β mRNA to promote ER-β expression. And Vigilin/ ER-β relieve the mitochondrial damage and cell apoptosis induced by PA through regulating CnA-mediated Drp1 signaling pathway, which revealed the mechanism and strategy of hypercholesterolemia in female infertility.

Methods

The ovarian granulosa cell-like human granulosa (KGN) cell line and the immortalized normal ovarian surface epithelial cell line (IOSE80) were used to verify the effect of PA on cell viability and apoptosis by MTT and flow cytometry assay, respectively. Then mitochondria damage was confirmed by mitochondrial membrane potential, mitochondrial ROS detection assay and western blot in KGN cells. Thorough luciferase reporter assay and RIP-qPCR, the relationship between vigilin and ER-β was investigated.

Results

In our study, PA induced mitochondrial damage-mediated cell apoptosis of KGN cells was dose-dependently, while PA shown no effects on in IOSE80 cells. Then the role of calcineurin (CnA)-mediated Drp1 signaling pathway on KGN cells was confirmed by treating with Mdivi-1 or FK506T. In addition, the changed level of vigilin and ER-β was observed in cell apoptosis of KGN cells induced by PA. By transfecting vigilin vector or ER-β vector into KGN cells, respectively, vigilin and ER-β were demonstrated to regulate the apoptosis of KGN cells. And vigilin was a binding protein of ER-β mRNA.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。