PPARGC1A型
下调和上调
细胞生物学
细胞生长
氧化应激
辅活化剂
线粒体
化学
过氧化物酶体
抗氧化剂
生物
受体
生物化学
基因
转录因子
作者
Shiyu An,Zifei Liu,M.A. El-Samahy,Mingtian Deng,Xiaoxiao Gao,Yaxu Liang,Chen-Bo Shi,Zhihai Lei,Feng Wang,Guomin Zhang
出处
期刊:Reproduction
[Bioscientifica]
日期:2021-03-10
卷期号:161 (5): 523-537
被引量:8
摘要
Long ncRNAs regulate a complex array of fundamental biological processes, while its molecular regulatory mechanism in Leydig cells (LCs) remains unclear. In the present study, we established the lncRNA LOC102176306/miR-1197-3p/peroxisome proliferator-activated receptor gamma coactivator 1 alpha ( PPARGC1A ) regulatory network by bioinformatic prediction, and investigated its roles in goat LCs. We found that lncRNA LOC102176306 could efficiently bind to miR-1197-3p and regulate PPARGC1A expression in goat LCs. Downregulation of lncRNA LOC102176306 significantly supressed testosterone (T) synthesis and ATP production, decreased the activities of antioxidant enzymes and mitochondrial complex I and complex III, caused the loss of mitochondrial membrane potential, and inhibited the proliferation of goat LCs by decreasing PPARGC1A expression, while these effects could be restored by miR-1197-3p inhibitor treatment. In addition, miR-1197-3p mimics treatment significantly alleviated the positive effects of lncRNA LOC102176306 overexpression on T and ATP production, antioxidant capacity and proliferation of goat LCs. Taken together, lncRNA LOC102176306 functioned as a sponge for miR-1197-3p to maintain PPARGC1A expression, thereby affecting the steroidogenesis, cell proliferation and oxidative stress of goat LCs. These findings extend our understanding of the molecular mechanisms of T synthesis, cell proliferation and oxidative stress of LCs.
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