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Cold-inducible RNA-binding protein regulates cyclin B1 against spermatogenesis arrest caused by heat stress

Heyu Liu1,2, Chengcheng Xu1, Meng Bao1

  • 1Institute of Reproductive Health, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Andrology
|October 10, 2021
PubMed
Abstract

Insights

Heat stress causes testicular damage. Cold-inducible RNA-binding protein (CIRBP) regulates spermatogenesis arrest by controlling cyclin B1 expression, protecting against heat-induced injury.

Area of Science:

  • Reproductive Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Heat stress induces spermatogenesis arrest and apoptosis in mouse testes.
  • Apoptosis is linked to reduced cold-inducible RNA-binding protein (CIRBP) expression.
  • CIRBP's role in spermatogenesis arrest and its regulatory mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the mechanism by which CIRBP contributes to heat stress-induced testicular spermatogenesis arrest.

Main Methods:

  • RNA sequencing of testicular tissue from heat-stressed and control mice.
  • Bioinformatics analysis to identify key mRNAs and pathways.
  • Validation of CIRBP-Ccnb1 interaction using western blotting, flow cytometry, and RNA pulldown assays.
  • Investigation in a mouse spermatocyte cell line (GC-2spd).

Main Results:

  • CIRBP-regulated mRNA changes were associated with cell cycle and RNA processing.
  • Cyclin B1 (Ccnb1) was identified as a key target, regulating the G2/M transition.
  • CIRBP directly binds to the 3'-untranslated region of Ccnb1 mRNA.
  • CIRBP regulates cyclin B1 expression, inhibiting spermatogenesis arrest.

Conclusions:

  • CIRBP plays a role in mitigating heat stress-induced testicular damage.
  • CIRBP regulates spermatogenesis arrest by controlling cyclin B1 expression.
  • Cyclin B1 inhibits spermatogenesis arrest, and CIRBP modulates this effect.
Keywords:
RNA-binding proteincell cyclecyclin B1heat stresstestis

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