Suppression of miR-1197-3p attenuates HO-induced apoptosis of goat luteinized granulosa cells via targeting PPARGC1A.

Authors:
Guo-Min Zhang
Guo-Min Zhang
The Second Affiliated Traditional and Western Medicine Hospital of Hunan University of Traditional Chinese Medicine
China
Yan-Li Zhang
Yan-Li Zhang
Nanjing Agricultural University
China
Yong-Jie Wan
Yong-Jie Wan
Nanjing Agricultural University
China
Zi-Yu Wang
Zi-Yu Wang
Nanjing Agricultural University
China
Shen-Hua Xiao
Shen-Hua Xiao
Jiangsu Livestock Embryo Engineering Laboratory
Fan-Xing Meng
Fan-Xing Meng
Jiangsu Livestock Embryo Engineering Laboratory

Theriogenology 2019 Jul 11;132:72-82. Epub 2019 Apr 11.

Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China. Electronic address:

Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PPARGC1A) acts as a powerful coactivator of many transcriptional factors that relate to granulosa cell (GC) apoptosis. In this study, the miRNAs mediating goat follicular atresia and luteinized granulosa cell (LGC) apoptosis induced by hydrogen peroxide (HO) via PPARGC1A were investigated. Our results showed that miR-1197-3p targeted PPARGC1A was predicted by bioinformatics algorithm and verified by luciferase reporter assay. In addition, miR-1197-3p promoted goat LGC apoptosis via PPARGC1A through mitochondrial-dependent apoptosis pathway, and these effects could be restored by PPARGC1A overexpression. Moreover, HO-induced LGC apoptosis significantly upregulated miR-1197-3p expression and downregulated PPARGC1A level. Pretreatment of miR-1197-3p inhibitor alleviated LGC apoptosis induced by 400 μM HO for 12 h, and preserved the mitochondrial membrane potential by increasing PPARGC1A expression. In conclusion, miR-1197-3p might act as an essential regulator of goat LGC apoptosis potentially via the mitochondrial-dependent apoptosis pathway by targeting PPARGC1A.

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Source
https://linkinghub.elsevier.com/retrieve/pii/S0093691X193009
Publisher Site
http://dx.doi.org/10.1016/j.theriogenology.2019.04.008DOI Listing

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July 2019
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