Opposite effects of monokines (interleukin-1 and tumor necrosis factor) on proliferation and heparin-binding (fibroblast) growth factor binding to human aortic endothelial and smooth muscle cells.

Heparin-binding (fibroblast) growth factors (HBGF) are mitogens for both human aortic endothelial and smooth muscle cells. Under similar conditions, both vascular cells display similar numbers of specific HBGF binding sites with similar apparent affinity for HBGF. The monokines, interleukin-1 and tumor necrosis factor, inhibit endothelial cell growth and stimulate smooth muscle cell growth. The opposite mitogenic effects correlate with reduction and increase in HBGF receptor number displayed by endothelial and smooth muscle cells, respectively. These results suggest that the two monokines may depress endothelial cell regeneration and augment smooth muscle cell hyperplasia by differential modulation of the HBGF receptor in the two vascular cell types.