Abstract
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.
MeSH Terms
Aorta/cytology,metabolism,ultrastructure
Cell Division/drug effects
Cells, Cultured
Endothelium, Vascular/cytology,metabolism,ultrastructure
Growth Substances/metabolism
Heparin/metabolism
Humans
Hyperplasia/metabolism,pathology
Interleukin-1/pharmacology
Monokines/pharmacology
Muscle, Smooth, Vascular/cytology,metabolism,ultrastructure
Receptors, Mitogen/drug effects,metabolism
Receptors, Vascular Endothelial Growth Factor
Tumor Necrosis Factor-alpha/pharmacology
Chemicals
Growth Substances
Interleukin-1
Monokines
Receptors, Mitogen
Tumor Necrosis Factor-alpha
Heparin
Receptors, Vascular Endothelial Growth Factor
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Sawada H
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946.
Kan M
McKeehan W L
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