Suppression of miR-1197–3p attenuates H2O2-induced apoptosis of goat luteinized granulosa cells via targeting PPARGC1A

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 (H2O2) 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, H2O2-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 H2O2 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. •miR-1197–3p promotes goat LGC apoptosis via directly targeting PPARGC1A.•400 μM H2O2 for 12 h treatment was the optimal condition for H2O2 induced goat LGC apoptosis model.•Suppression of miR-1197–3p attenuated H2O2-induced LGC apoptosis by targeting PPARGC1A.