Chronic stress inhibits testosterone synthesis in Leydig cells through mitochondrial damage via Atp5a1.
Xiaofan XiongQiuhua WuLingyu ZhangShanfeng GaoRufeng LiLin HanMeiyang FanMiaomiao WangLiying LiuXiaofei WangChunli ZhangYanlong XinZongfang LiChen HuangJuan YangPublished in: Journal of cellular and molecular medicine (2021)
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.
Keyphrases
- induced apoptosis
- cell cycle arrest
- poor prognosis
- oxidative stress
- replacement therapy
- endoplasmic reticulum stress
- stress induced
- mass spectrometry
- type diabetes
- metabolic syndrome
- binding protein
- adipose tissue
- skeletal muscle
- long non coding rna
- amino acid
- molecular dynamics
- density functional theory
- polycystic ovary syndrome