Effect of tunicamycin on the turnover of epidermal growth factor receptors in cultured calf aorta smooth muscle cells. Comparison with IMR-90 human lung fibroblasts.
Treatment of cultured calf aorta smooth muscle cells with tunicamycin, a potent inhibitor of dolichol-mediated glycosylation, resulted in progressive loss of receptors for epidermal growth factor with 50% of receptors lost after 6 h. Receptor half-life was also 6 h with cycloheximide treatment but was 12 h with either actinomycin D or camptothesin treatment. The epidermal growth factor-induced processing (internalization and/or degradation) of residual receptors remaining after tunicamycin treatment appeared to be unaltered. 50% decrease in 125I-labeled epidermal growth factor binding was observed also with IMR-90 fibroblasts upon 6 h treatment with tunicamycin, although these cells were less sensitive to inhibition by tunicamycin of glycosylation and protein synthesis.
D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism; D001665:Binding Sites / Q000187:drug effects; D002166:Camptothecin / Q000494:pharmacology; D002417:Cattle; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004815:Epidermal Growth Factor / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism; D005944:Glucosamine / Q000031:analogs & derivatives*; D006207:Half-Life; D006801:Humans; D008168:Lung / Q000378:metabolism; D008297:Male; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D010455:Peptides / Q000378:metabolism*; D014415:Tunicamycin / Q000494:pharmacology*
D010455:Peptides; D014415:Tunicamycin; D003609:Dactinomycin; D004815:Epidermal Growth Factor; D003513:Cycloheximide; D005944:Glucosamine; D002166:Camptothecin