Basic FGF’s role in smooth muscle cell proliferation: A basis for molecular atherectomy

Abstract

Migration and proliferation of smooth muscle cells (SMC) in the arterial intima are well recognized features of atherosclerosis [1] and are especially prominent features of transplant atherosclerosis [2], and of restenosis after balloon angioplasty [3,4] or coronary bypass grafting [5]. The proliferation of vascular SMC may also be important in Kaposi’s sarcoma [6] and in some types of hypertension [7–10]. In atherosclerosis and in restenosis, factors implicated in the migration and proliferation of SMC include thrombi [11–13], lipoproteins [14–16], stretch [17–21], reduced flow and shear [17–21], and loss of endothelial-derived growth inhibitors [22–26]. In addition, the SMC themselves can express mitogenic vasoconstrictors [27–29], such as angiotensin, and platelet-derived growth factors (PDGFs) [30–35]. Various PDGF dimers are also released by platelets, macrophages and endothelial cells [30–35]. The possibility of a similar role for basic fibroblast growth factor (bFGF), a heparin-binding 18 kD peptide best known for its angiogenic, neurotropic, and mesoderm-inducing effects [36–38], has only recently been considered.