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慢性应激通过 Atp5a1 导致线粒体损伤从而抑制睾丸间质细胞中睾酮的合成。

Chronic stress inhibits testosterone synthesis in Leydig cells through mitochondrial damage via Atp5a1.

机构信息

Western China Science and Technology Innovation Port in Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Department of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.

出版信息

J Cell Mol Med. 2022 Jan;26(2):354-363. doi: 10.1111/jcmm.17085. Epub 2021 Dec 10.

DOI:10.1111/jcmm.17085
PMID:34894202
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8743653/
Abstract

Stress is one of the leading causes of male infertility, but its exact function in testosterone synthesis has scarcely been reported. We found that adult male rats show a decrease in bodyweight, genital index and serum testosterone level after continual chronic stress for 21 days. Two-dimensional gel electrophoresis (2-DE) and MALDI-TOF-MS analysis identified 10 differentially expressed proteins in stressed rats compared with controls. A strong protein interaction network was found to be centred on Atp5a1 among these proteins. Atp5a1 expression significantly decreased in Leydig cells after chronic stress. Transfection of Atp5a1 siRNAs decreased StAR, CYP11A1, and 17β-HSD expression by damaging the structure of mitochondria in TM3 cells. This study confirmed that chronic stress plays an important role in testosterone synthesis by regulating Atp5a1 expression in Leydig cells.

摘要

压力是导致男性不育的主要原因之一，但它在睾丸酮合成中的具体作用却鲜有报道。我们发现，成年雄性大鼠在连续慢性应激 21 天后，体重、生殖器指数和血清睾丸酮水平均下降。与对照组相比，通过二维凝胶电泳（2-DE）和 MALDI-TOF-MS 分析，在应激大鼠中鉴定出 10 种差异表达蛋白。在这些蛋白中，一个以 Atp5a1 为中心的强蛋白相互作用网络被发现。慢性应激后，Leydig 细胞中的 Atp5a1 表达明显下降。在 TM3 细胞中，Atp5a1 的 siRNA 转染通过破坏线粒体的结构，降低了 StAR、CYP11A1 和 17β-HSD 的表达。本研究证实，慢性应激通过调节 Leydig 细胞中 Atp5a1 的表达，在睾丸酮合成中起着重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/8e1e9a3b9ac7/JCMM-26-354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/5a21648407f8/JCMM-26-354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/ca6aa243e1fb/JCMM-26-354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/b9b5a505db84/JCMM-26-354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/debbd42ec78d/JCMM-26-354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/8e1e9a3b9ac7/JCMM-26-354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/5a21648407f8/JCMM-26-354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/ca6aa243e1fb/JCMM-26-354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/b9b5a505db84/JCMM-26-354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/debbd42ec78d/JCMM-26-354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8f/8743653/8e1e9a3b9ac7/JCMM-26-354-g005.jpg

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