Thrombin induces rapid PAR1-mediated non-classical FGF1 release

Biochem Biophys Res Commun. 2006 Nov 24;350(3):604-9. doi: 10.1016/j.bbrc.2006.09.107. Epub 2006 Sep 28.

Abstract

Thrombin induces cell proliferation and migration during vascular injury. We report that thrombin rapidly stimulated expression and release of the pro-angiogenic polypeptide fibroblast growth factor 1 (FGF1). Thrombin failed to induce FGF1 release from protease-activated receptor 1 (PAR1) null fibroblasts, indicating that this effect was dependent on PAR1. Similarly to thrombin, FGF1 expression and release were induced by TRAP, a specific oligopeptide agonist of PAR1. These results identify a novel aspect of the crosstalk between FGF and thrombin signaling pathways which both play important roles in tissue repair and angiogenesis.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Dose-Response Relationship, Drug
  • Fibroblast Growth Factor 1 / metabolism*
  • Mice
  • NIH 3T3 Cells
  • Receptor, PAR-1 / metabolism*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Thrombin / administration & dosage*

Substances

  • Receptor, PAR-1
  • Fibroblast Growth Factor 1
  • Thrombin