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

Theriogenology

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

Published: July 2019

AI Article Synopsis

  • PPARGC1A is a key coactivator for transcription factors involved in the apoptosis of granulosa cells, especially in the context of hydrogen peroxide exposure.
  • Research identified miR-1197-3p as a microRNA that targets PPARGC1A, promoting the apoptosis of luteinized granulosa cells via a mitochondrial-dependent mechanism.
  • Inhibiting miR-1197-3p before hydrogen peroxide treatment was found to reduce cell apoptosis by restoring PPARGC1A levels and maintaining mitochondrial membrane potential.

Article Abstract

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
http://dx.doi.org/10.1016/j.theriogenology.2019.04.008DOI Listing

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