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Related Experiment Videos

Versican mediates mesenchymal-epithelial transition.

Wang Sheng1, Guizhi Wang, David P La Pierre

  • 1Sunnybrook and Women's College Health Sciences Centre, Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.

Molecular Biology of the Cell
|February 3, 2006
PubMed
Summary
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Versican V1 isoform induces mesenchymal-epithelial transition (MET) in fibroblasts. Reducing versican expression inhibits MET in kidney cells, demonstrating versican

Area of Science:

  • Cell Biology
  • Extracellular Matrix Biology

Background:

  • Versican is a proteoglycan involved in cell adhesion and migration.
  • Alternative splicing creates multiple versican isoforms with distinct functions.

Purpose of the Study:

  • To investigate the role of versican V1 isoform in mesenchymal-epithelial transition (MET).

Main Methods:

  • Ectopic expression of versican V1 in NIH3T3 fibroblasts.
  • Inhibition of endogenous versican in metanephric mesenchyme.
  • Analysis of cell morphology, cytoskeleton, and gene expression (cadherin switch, occludin).
  • Methylation-specific PCR (MSP) to assess N-cadherin promoter methylation.

Main Results:

  • Versican V1 expression induced MET, characterized by morphological changes and altered cell architecture.

Related Experiment Videos

  • V1 promoted an N-cadherin to E-cadherin switch, leading to epithelial adhesion.
  • V1 reduced vimentin and increased occludin expression, promoting cell polarization.
  • N-cadherin promoter methylation suppressed N-cadherin expression; exogenous N-cadherin reversed V1's effects.
  • Silencing versican inhibited MET in both NIH3T3 cells and metanephric mesenchyme.

    • Conclusions:

    • Versican V1 isoform is sufficient to induce MET in fibroblasts.
    • Versican plays a crucial role in regulating MET in developmental contexts like kidney development.