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Inhibitors of c-Jun phosphorylation impede ovine primordial follicle activation

Michael J Bertoldo1, Jérémy Bernard2, Nicolas Duffard2

  • 1INRA, UMR85 Physiologie de la Reproduction et des Comportements, Nouzilly 37380, France School of Women's and Children's Health, Discipline of Obstetrics and Gynaecology, University of New South Wales, Sydney, Australia michael.bertoldo@unsw.edu.au.

Molecular Human Reproduction
|February 25, 2016
PubMed
Abstract

Insights

The c-Jun-N-terminal kinase (JNK) pathway is implicated in primordial follicle activation. Inhibiting this pathway with specific drugs impeded follicle activation and reduced cell proliferation, offering insights into fertility preservation.

Area of Science:

  • Reproductive biology
  • Cell signaling pathways

Background:

  • Primordial follicle activation is crucial for fertility preservation but poorly understood.
  • The JNK pathway is essential for cell cycle and pre-antral follicle development in mice.

Purpose of the Study:

  • To investigate the role of the JNK pathway in primordial follicle activation.
  • To assess the impact of JNK inhibitors on ovarian cortex cultures.

Main Methods:

  • Ovine ovarian cortex was cultured with JNK inhibitors (SP600125, JNK inhibitor VIII) and AMH.
  • Follicular morphometry, PCNA, apoptosis, and Foxo3a were assessed via immunohistochemistry.

Main Results:

  • SP600125, JNK inhibitor VIII, and AMH significantly inhibited primordial follicle activation.
  • Reduced PCNA expression indicated decreased somatic cell proliferation.
  • High inhibitor concentrations induced follicular apoptosis.

Conclusions:

  • The JNK pathway plays a significant role in primordial follicle activation.
  • Inhibiting JNK signaling can impede follicle activation and proliferation.
  • Findings have implications for fertility preservation strategies.
Keywords:
Foxo3aanti-Mullerian hormonec-Jun-N-terminal kinasefertility preservationin vitro ovarian tissue cultureprimordial follicle activation

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