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

  • Xiaofan Xiong
  • , Qiuhua Wu
  • , Lingyu Zhang
  • , Shanfeng Gao
  • , Rufeng Li
  • , Lin Han
  • , Meiyang Fan
  • , Miaomiao Wang
  • , Liying Liu
  • , Xiaofei Wang
  • , Chunli Zhang
  • , Yanlong Xin
  • , Zongfang Li
  • , Chen Huang
  • , Juan Yang

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

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.

Original languageEnglish
Pages (from-to)354-363
Number of pages10
JournalJournal of Cellular and Molecular Medicine
Volume26
Issue number2
DOIs
StatePublished - Jan 2022

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