Thrombin induces rapid PAR1-mediated non-classical FGF1 release.
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.
Duarte
Maria
M
Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME 04074, USA.
Kolev
Vihren
V
Soldi
Raffaella
R
Kirov
Alexander
A
Graziani
Irene
I
Oliveira
Silvia Marta
SM
Kacer
Doreen
D
Friesel
Robert
R
Maciag
Thomas
T
Prudovsky
Igor
I
D000818:Animals; D004305:Dose-Response Relationship, Drug; D016220:Fibroblast Growth Factor 1 / Q000378:metabolism*; D051379:Mice; D041681:NIH 3T3 Cells; D044463:Receptor, PAR-1 / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D013917:Thrombin / Q000008:administration & dosage*
D044463:Receptor, PAR-1; D016220:Fibroblast Growth Factor 1; D013917:Thrombin