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Shi-Yu An Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China

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Zi-Fei Liu Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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El-Samahy M A Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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Ming-Tian Deng Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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Xiao-Xiao Gao Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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Ya-Xu Liang Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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Chen-Bo Shi Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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Zhi-Hai Lei College of veterinary medicine, Nanjing Agricultural University, Nanjing, China

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Feng Wang Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China

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Guo-Min Zhang Jiangsu Livestock Embryo Engineering Laboratory, Nanjing Agricultural University, Nanjing, China
College of veterinary medicine, Nanjing Agricultural University, Nanjing, China

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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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