miR-181a increases FoxO1 acetylation and promotes granulosa cell apoptosis via SIRT1 downregulation.
Document Type
Article
Publication Date
10-5-2017
Abstract
Oxidative stress impairs follicular development by inducing granulosa cell (GC) apoptosis, which involves enhancement of the transcriptional activity of the pro-apoptotic factor Forkhead box O1 (FoxO1). However, the mechanism by which oxidative stress promotes FoxO1 activity is still unclear. Here, we found that miR-181a was upregulated in hydrogen peroxide (H
Recommended Citation
Zhang, Mei; Zhang, Qun; Hu, Yali; Xu, Lu; Jiang, Yue; Zhang, Chunxue; Ding, Lijun; Jiang, Ruiwei; Sun, Jianxin; Sun, Haixiang; and Yan, Guijun, "miR-181a increases FoxO1 acetylation and promotes granulosa cell apoptosis via SIRT1 downregulation." (2017). Center for Translational Medicine Faculty Papers. Paper 49.
https://jdc.jefferson.edu/transmedfp/49
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
28981116
Language
English
Comments
This article has been peer reviewed. It is the author’s final published version in Cell Death & Disease, Volume 8, Issue 10, October 2017, Page e3088.
The published version is available at https://doi.org/10.1038/cddis.2017.467. Copyright © Zhang et al.