Role of basic fibroblast growth factor in proliferation of endothelium and smooth muscle after denuding injury in vivo.

Abstract

Balloon catheter injury of the rat common carotid artery causes complete denudation of endothelium. Using this model, endothelial regrowth from the aortic arch and the carotid bifurcation is initially rapid but cessation of endothelial outgrowth occurs after approximately 6 weeks [1]. This leaves a central portion of the common carotid artery permanently denuded of endothelium. However, if a less traumatic technique (filament loop denudation) is used to remove the endothelium, proliferation of endothelium proceeds at a continuously high rate until complete coverage of the vessel is achieved within approximately 12 weeks. The difference in endothelial regrowth in these two models allowed us to investigate which factors might be involved in controlling the growth of these cells. With an antibody raised against human recombinant basic fibroblast growth factor (bFGF) immunocytochemistry was performed on en face (Häutchen) preparations of the leading edge of the regenerating endothelium. Strong staining with this antibody was found only in those endothelial cells that continued to proliferate, i.e. at early times after balloon catheter denudation and at all times after filament denudation [1]. The staining appeared to be predominantly nuclear. Endothelial cells that had stopped proliferating, i.e. at later times after balloon catheter injury or normal endothelium in uninjured vessels showed markedly less staining.KeywordsBasic Fibroblast Growth FactorEndothelial Cell ProliferationSmooth Muscle Cell ProliferationIntimal ThickeningNormal EndotheliumThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.