Glucocorticoids induce a 29 000 Mr protein in DDT1 MF-2 smooth muscle cells but not in the DDT1 MF-2 GR glucocorticoid resistant variant.
We have demonstrated that glucocorticoids induce in DDT1 MF-2 cells by a glucocorticoid mediated mechanism the synthesis of a methionine-cysteine rich protein of 29 000 Mr (p29). Induction of p29 is not observed in DDT1 MF-2 GR glucocorticoid resistant variants which have only 7% of glucocorticoid receptor site per cell compared to wild type cells. Increased synthesis of p29 is specific to glucocorticoids since neither androgens, estrogens, progesterone nor the glucocorticoid antagonist dexamethasone mesylate are effective inducers. Stimulation of p29 synthesis in wild type cells is observed at 10(-10) M triamcinolone acetonide, reaching a maximum at a concentration of 1 X 10(-8) M. The induction of p29 is not a function of glucocorticoid arrest of DDT1 MF-2 cells since DDT1 MF-2 cells promoted to re-enter the cell cycle by 50 ng/ml platelet derived growth factor (PDGF) continue synthesis of p29. Finally, increased levels of p29 translation products are observed in cell free translation assays carried out utilizing poly A+ RNA transcripts isolated from glucocorticoid treated cells. These data suggest that the glucocorticoid stimulation of p29 synthesis is a transcriptional and/or RNA processing event controlled by glucocorticoid receptor complexes.
D000818:Animals; D004351:Drug Resistance; D014644:Genetic Variation; D007700:Kinetics; D008970:Molecular Weight; D009124:Muscle Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000302:isolation & purification; D009130:Muscle, Smooth / Q000378:metabolism*; D014176:Protein Biosynthesis; D011817:Rabbits; D012156:Reticulocytes / Q000378:metabolism; D014222:Triamcinolone Acetonide / Q000494:pharmacology*
D009124:Muscle Proteins; D014222:Triamcinolone Acetonide