Factors controlling the development of arterial lesions after injury.

This review discusses the role of growth factors on the proliferation of smooth muscle cells (SMCs) in injured arteries. We have used a variety of procedures to injure rat carotid arteries and noted that removal of endothelium followed by platelet adherence does not always initiate SMC replication. Furthermore, thrombocytopenia did not reduce the early SMC replication induced by balloon catheter injury. Platelet-derived growth factor (PDGF) has been found to exert little effect on SMC replication but markedly influences the ability of SMCs to migrate to the intima. Basic fibroblast growth factor (bFGF) is a potent mitogen for SMCs in denuded arteries while having no effect on cells in control uninjured arteries. We have hypothesized that arterial injury leads to release of bFGF from injured SMCs and so stimulates cell replication. Rats were treated with antibodies to bFGF immediately before balloon injury, and this significantly reduced the SMC replication. These findings suggest that in vivo bFGF is an important mitogen for initiating SMC replication and that PDGF is important as a chemotactic for SMCs.