Effect of PGC-1α overexpression or silencing on mitochondrial apoptosis of goat luteinized granulosa cells.
作者： Guo-Min Zhang , Ming-Tian Deng , Yan-Li Zhang , Yi-Xuan Fan , Yong-Jie Wan
DOI: 10.1007/S10863-016-9684-6
关键词:
摘要: During goat follicular development, abnormal expression of peroxisome proliferator- activated receptor gamma coactivator-1 alpha (PGC-1α) in granulosa cells (GCs) may contribute to atresia with unknown regulatory mechanisms. In this study, we investigate the effect ectopic or interference PGC-1α on cell apoptosis first passage (FGCs) vitro. The results indicate that silencing by short hairpin RNA (shRNA) FGCs significantly reduced mitochondrial DNA (mtDNA) copy number (P < 0.05), changed mitochondria ultrastructure, and induced (P < 0.05). transcription translation levels apoptosis-related genes BCL-2-associated X protein (BAX), caspase 3, 9 were up-regulated (P < 0.05, respectively). Moreover, ratio BAX/B-cell lymphoma 2 (BCL-2) was release cytochrome c (cyt c) lactate dehydrogenase (LDH) enhanced respectively) FGCs. Furthermore, anti-oxidative related superoxide dismutase (SOD2), glutathione peroxidase (GPx) catalase (CAT) down-regulated activity glutathione/glutathione disulfide (GSH/GSSG) inhibited While enforced increased involved regulation function biogenesis, anti-apoptosis capacity. Taken together, our reveal lack lead dysfunction disrupt cellular redox balance, thus resulting GCs through mitochondria-dependent apoptotic pathway.
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