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Related Experiment Videos

Basic FGF increases communication between cells of the developing neocortex

B Nadarajah1, H Makarenkova, D L Becker

  • 1Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 19, 1998
PubMed
Summary
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Basic fibroblast growth factor (bFGF) increases connexin 43 (Cx43) expression and mRNA in cortical progenitor cells. This suggests bFGF signaling via receptor tyrosine kinases regulates cell proliferation through gap junctions during corticogenesis.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Cortical progenitor cells are crucial for brain development.
  • Gap junctions facilitate intercellular communication.
  • Basic fibroblast growth factor (bFGF) is a key signaling molecule.

Purpose of the Study:

  • To investigate the effect of bFGF on gap junction protein expression in cortical progenitor cells.
  • To elucidate the signaling pathways involved in bFGF-mediated changes in Cx43.
  • To understand the functional consequences of bFGF on intercellular communication and proliferation.

Main Methods:

  • In vitro culture of cortical progenitor cells.
  • Quantitative analysis of connexin 43 (Cx43) mRNA and protein expression.

Related Experiment Videos

  • Investigation of receptor tyrosine kinase (RTK) pathway involvement.
  • Assessment of intercellular dye-coupling to measure gap junction function.
  • Main Results:

    • bFGF treatment significantly increased Cx43 expression and mRNA levels in both proliferating and nonproliferating cells.
    • The observed increase in Cx43 is likely due to enhanced gene transcription.
    • bFGF-induced Cx43 upregulation is mediated by the RTK pathway.
    • Enhanced Cx43 expression correlated with increased intercellular dye-coupling via gap junctions.

    Conclusions:

    • bFGF signaling upregulates Cx43 expression in cortical progenitor cells.
    • Gap junction channels play a role in mediating the proliferative effects of bFGF during corticogenesis.
    • This study reveals a novel mechanism by which bFGF influences neural development through gap junction modulation.