Androgen stimulated elevation in androgen receptor levels is inhibited by the synthetic glucocorticoid triamcinolone acetonide.
Two cloned tumor cell lines derived from the rat prostate and hamster ductus deferens contain receptors for androgens and glucocorticoids. Androgens increase both the rate of proliferation in these cells and induce a doubling in the number of androgen receptors within 6 hours. This elevation in androgen receptors is dependent on protein synthesis. The glucocorticoid triamcinolone acetonide specifically inhibits both these androgen mediated events without altering the equilibrium dissociation constant (Kd) of the androgen receptor for either [3H]-methyltrienolone (Kd = 0.46 nM) or [3H]-dihydrotestosterone (Kd = 0.2 nM). These observations infer that androgen receptor up-regulation is an important facet of androgen action which may be modulated by glucocorticoids.
D000728:Androgens / Q000494:pharmacology*; D000818:Animals; D002460:Cell Line; D002999:Clone Cells; D006224:Cricetinae; D013196:Dihydrotestosterone / Q000378:metabolism; D004963:Estrenes / Q000378:metabolism; D007700:Kinetics; D008297:Male; D015741:Metribolone; D011471:Prostatic Neoplasms / Q000378:metabolism*; D051381:Rats; D011944:Receptors, Androgen / Q000187:drug effects / Q000378:metabolism*; D011987:Receptors, Steroid / Q000378:metabolism*; D045165:Testosterone Congeners / Q000378:metabolism; D014222:Triamcinolone Acetonide / Q000494:pharmacology*
D000728:Androgens; D004963:Estrenes; D011944:Receptors, Androgen; D011987:Receptors, Steroid; D045165:Testosterone Congeners; D013196:Dihydrotestosterone; D015741:Metribolone; D014222:Triamcinolone Acetonide