Ultraviolet-B (290-320 nm)-irradiation inhibits epidermal growth-factor binding to mammalian cells.
Mitogens, such as polypeptide growth factors and phorbol ester tumor promoters, act by binding to specific receptors and inducing a pleiotropic response in cultured mammalian cells, which results in the induction of cellular proliferation. An early effect of such agents is the inhibition of binding of epidermal growth factor (EGF) to its receptor. Ultraviolet radiation has also been shown to induce a proliferative response in vivo and in vitro and to act as a tumor promoter in animal skin. We, therefore, examined the effect of ultraviolet radiation (UVB - 290-320 nm) on EGF binding to cells in culture. We found that UVB (100-300 J/m2) induced a rapid, dose-dependent inhibition of EGF binding in a mouse fibroblast cell line, which resulted from a decrease in both number and affinity of binding sites. Phosphorylation of the EGF receptor by protein kinase C (PKC) is not likely to be the mechanism for inhibition, since UVB treatment did not result in PKC activation or modulation of phorbol diester binding.
Matsui
M S
MS
Department of Dermatology, Columbia University, New York, New York 10032.
Laufer
L
L
Scheide
S
S
DeLeo
V
V
D000818:Animals; D002478:Cells, Cultured; D004789:Enzyme Activation / Q000528:radiation effects; D004815:Epidermal Growth Factor / Q000378:metabolism / Q000528:radiation effects*; D005347:Fibroblasts / Q000378:metabolism / Q000528:radiation effects*; D011493:Protein Kinase C / Q000378:metabolism; D014466:Ultraviolet Rays
D004815:Epidermal Growth Factor; D011493:Protein Kinase C