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Cypermethrin triggers YY1-mediated testosterone biosynthesis suppression.

Changjiang Liu1, Jiayuan Qu2, Mingzhu Wu3

  • 1NHC Key Laboratory of Birth Defects and Reproductive Health, Chongqing Population and Family Planning Science and Technology Research Institute, 420 Baohuan Road, Chongqing 400020, China; Medical Research Institute, Southwest University, Chongqing 400715, China.

Ecotoxicology and Environmental Safety
|September 20, 2021
PubMed
Summary

Cypermethrin pesticide exposure suppresses testosterone production by disrupting the lncRNA XIST/miR-142-5p axis, impacting the Jak/Stat pathway and steroidogenic genes in Leydig cells.

Keywords:
CypermethrinJak1/Stat1 pathwayNon-coding RNAsTestosterone biosynthesis suppressionYY1

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Toxicology

Background:

  • Cypermethrin (CYP) is a widely used pesticide with endocrine-disrupting properties, particularly anti-androgenicity.
  • The mechanisms underlying CYP-induced testosterone suppression, involving non-coding RNAs and signaling pathways, require further elucidation.

Purpose of the Study:

  • To investigate the roles of non-coding RNAs and the Janus kinase/Signal transducer and activator of transcription (Jak/Stat) pathway in cypermethrin-mediated suppression of testosterone biosynthesis.
  • To elucidate the molecular mechanisms by which cypermethrin affects Leydig cell function and steroidogenesis.

Main Methods:

  • Utilized Sprague-Dawley (SD) rats and isolated Leydig cells exposed to cypermethrin (β-CYP).
  • Assessed plasma testosterone levels, testicular histomorphology, and ultrastructural changes.
  • Quantified expression of lncRNA XIST and miR-142-5p.
  • Performed co-immunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), quantitative polymerase chain reaction (qPCR), and gene knockdown/overexpression assays.

Main Results:

  • β-CYP exposure decreased testosterone levels and induced testicular abnormalities.
  • β-CYP inhibited lncRNA XIST expression while inducing miR-142-5p expression in Leydig cells.
  • Overexpressed miR-142-5p targeted Jak1, dampening the Jak1/Stat1 pathway.
  • The Jak1/Stat1 pathway positively regulated transcription factors NFκB and YY1, which were impeded by β-CYP.
  • NFκB interacted with and modulated YY1, which in turn regulated steroidogenic genes StAR and 3β-HSD.

Conclusions:

  • The lncRNA XIST/miR-142-5p axis plays a critical role in cypermethrin's anti-androgenic effects.
  • Cypermethrin disrupts testosterone production by targeting the Jak1/Stat1 pathway via the lncRNA XIST/miR-142-5p interaction, subsequently affecting NFκB, YY1, and steroidogenic gene expression (StAR, 3β-HSD) in Leydig cells.