FSH protects mouse granulosa cells from oxidative damage by repressing mitophagy

• DOI: 10.1038/srep38090
• Publication Date: 2016-11-30T10:37:07Z
• Authors: Ming Shen; Yi Jiang; Zhiqiang Guan; Yan Cao; Shao-chen Sun; Honglin Liu
• Keywords: PINK1

Abstract Oxidative stress has been implicated in triggering granulosa cell (GC) death during follicular atresia. Recent studies suggested that follicle-stimulating hormone (FSH) a pivotal role protecting GCs from oxidative injury, although the exact mechanism remains largely unknown. Here, we report FSH promotes GC survival by inhibiting stress-induced mitophagy. The loss of viability caused was significantly reduced after treatment, which correlated with impaired activation mitophagy upon stress. Compared blocking displayed approximate preventive effect on death, but did not further restore cells pretreated inhibitor. Importantly, suppressed induction serine/threonine kinase PINK1 This inhibited mitochondrial translocation E3 ligase Parkin, is required for subsequent clearance mitochondria, and ultimately via In addition, knocking down using RNAi confirmed FSH-PINK1-Parkin-mitophagy pathway regulating under conditions. These findings introduce novel physiological function against damage targeting PINK1-Parkin-mediated