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The canonical WNT2 pathway and FSH interact to regulate gap junction assembly in mouse granulosa cells

Hong-Xing Wang1, Carolina Gillio-Meina, Shuli Chen

  • 1Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.

Biology of Reproduction
|July 12, 2013
PubMed

Insights

The WNT2/CTNNB1 pathway regulates connexin43 (CX43) expression and gap-junctional intercellular communication (GJIC) in granulosa cells. This pathway is crucial for follicle-stimulating hormone (FSH) to enhance GJIC during ovarian development.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Molecular Biology

Background:

  • WNTs are extracellular signals acting via Frizzled (FZD) receptors.
  • WNT2/CTNNB1 signaling regulates granulosa cell proliferation.
  • Connexin43 (CX43) gap junctions are vital for ovarian follicle development.

Purpose of the Study:

  • To investigate if WNT2 regulates CX43 expression and gap-junctional intercellular communication (GJIC) in granulosa cells.
  • To determine the role of the WNT2/CTNNB1 pathway in CX43 localization and GJIC.
  • To elucidate the interaction between WNT2/CTNNB1 signaling and follicle-stimulating hormone (FSH) in regulating GJIC.

Main Methods:

  • Small interfering RNA (siRNA) mediated knockdown of WNT2 and CTNNB1.
  • Quantitative assessment of CX43 expression.
  • Measurement of gap-junctional intercellular communication (GJIC) using established assays.
  • Immunofluorescence microscopy to analyze CTNNB1 localization.

Main Results:

  • WNT2 knockdown significantly reduced CX43 expression and GJIC.
  • CTNNB1 knockdown diminished CX43 expression, gap junction membrane presence, and GJIC.
  • WNT2 knockdown caused CTNNB1 to disappear from granulosa cell membranes.
  • CTNNB1 knockdown impaired FSH-induced CX43 mobilization into gap junctions.

Conclusions:

  • The WNT2/CTNNB1 pathway is a key regulator of CX43 expression and GJIC in granulosa cells.
  • This pathway modulates CTNNB1 stability and localization, impacting adherens junctions.
  • WNT2/CTNNB1 signaling is essential for FSH to stimulate GJIC, critical for ovarian follicle development.
Keywords:
adherens junctionbeta-cateninconnexin43gap junctionovarian folliculogenesis

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