ENDOTHELIN-1-SELECTIVE BINDING-SITES ARE DOWN-REGULATED BY TRANSFORMING GROWTH-FACTOR-BETA AND UP-REGULATED BY BASIC FIBROBLAST GROWTH-FACTOR IN A VASCULAR SMOOTH MUSCLE-DERIVED CELL-LINE
C. Cristiani et al., ENDOTHELIN-1-SELECTIVE BINDING-SITES ARE DOWN-REGULATED BY TRANSFORMING GROWTH-FACTOR-BETA AND UP-REGULATED BY BASIC FIBROBLAST GROWTH-FACTOR IN A VASCULAR SMOOTH MUSCLE-DERIVED CELL-LINE, Journal of cardiovascular pharmacology, 23(6), 1994, pp. 988-994
Endothelins (ETs) elicit in vivo and in vitro a potent vasoconstrictor
activity after binding to high-affinity receptors on vascular smooth
muscle cells (VSMC). A617 cells, a VSM-derived cell line, were used as
an in vitro model system to study selected growth factors and cytokin
es involved in proliferative and/or inflammatory diseases of the vesse
l wall as possible regulators of the high-affinity binding capacity of
ET-1 to the cells. Radioligand studies characterized the binding of E
T-1 to the isopeptide selective ET(A) receptor subtype on A617 cells a
s a time- and temperature-dependent saturable process (K-d = 0.13 +/-
0.04 nM, B-max = 49 +/- 7 fmol/10(6) cells). Pretreatment of A617 cell
s with basic fibroblast growth factor (bFGF), a mitogenic agent for va
scular cells, resulted in a time- and dose-dependent increase in ET-1
binding capacity, whereas preexposure to transforming growth factor-be
ta (TGF-beta) induced a reduction of the B-max for ET-1. Platelet-deri
ved growth factor (PDGF), interleukin-6 (IL-6), tumor necrosis factor-
alpha, and fetal bovine serum (FBS) pretreatments did not affect conse
quent ET-1 binding to A617 cells.