Interference with endogenous ras function inhibits cellular responses to wounding

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R G Sosnowski1, S Feldman, J R Feramisco

  • 1Department of Pharmacology, University of California, San Diego, La Jolla 92093-0636.

The Journal of Cell Biology
|April 1, 1993
PubMed

Insights

Cellular ras proteins are crucial for wound repair. Inhibiting ras signaling in bovine corneal endothelium cells blocked key repair responses like Fos expression and DNA synthesis after wounding.

Area of Science:

  • Cellular biology
  • Molecular biology
  • Tissue repair mechanisms

Background:

  • Tissue injury triggers cellular responses essential for repair, including gene induction, migration, and proliferation.
  • Cellular ras proteins are known regulators of growth factor signaling, but their role in wound healing is not fully understood.

Purpose of the Study:

  • To investigate the involvement of cellular ras proteins in the cellular response to tissue wounding.
  • To determine if ras signaling is essential for key wound repair processes in corneal endothelial cells.

Main Methods:

  • Utilized quiescent bovine corneal endothelium (BCE) cells in a tissue culture model.
  • Microinjected BCE cells with a dominant-interfering ras mutant protein (N17) or control proteins.
  • Stimulated cells with mechanical wounding and analyzed cellular responses.

Main Results:

  • Microinjection of dominant-interfering ras protein significantly inhibited the wound healing response.
  • Inhibition of ras signaling led to diminished Fos expression, a marker of AP-1 regulated genes.
  • Ras inhibition also blocked cell migration and DNA synthesis, crucial for tissue repair.

Conclusions:

  • Cellular ras proteins play a critical role in mediating the cellular responses to mechanical wounding.
  • Ras signaling is essential for the induction of gene expression, cell migration, and proliferation during wound repair.
  • Targeting ras pathways may offer therapeutic potential for enhancing wound healing.

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