Calcium dependence of glucocorticoid-induced lymphocytolysis.
A potent glucocorticoid, triamcinolone acetonide (9alpha-fluoro-11beta, 16alpha,17alpha, 21-tetrahydroxypregna-1,4-diene-3,20-dione-16,17-acetonide) and a divalent cation ionophore (A23187) had similar effects in vitro on [3H]uridine uptake and on lysis of thymocytes of adrenalectomized rats. Removal of Ca2+ from the medium blunted the cytolytic action of triamcinolone acetonide and virtually eliminated that of A23187. In Ca2+-free media, treatment of the thymocytes for 15 hr with triamcinolone acetonide or A23187 followed by re-introduction of Ca2+ resulted in a rapid decrease in cell survival. Based on the time courses of the responses, triamcinolone acetonide and A23187 evoked proportionate increases in 45Ca uptake and lysis of the thymocytes. These findings implicate enhanced Ca2+ uptake in glucocorticoid-dependent lymphocytolysis.
D015065:17-Hydroxycorticosteroids / Q000494:pharmacology*; D000315:Adrenalectomy; D000818:Animals; D001693:Biological Transport, Active; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D003350:Cortodoxone / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology*; D007700:Kinetics; D008214:Lymphocytes / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D011374:Progesterone / Q000494:pharmacology*; D051381:Rats; D014158:Transcription, Genetic; D014222:Triamcinolone Acetonide / Q000494:pharmacology*; D014529:Uridine / Q000378:metabolism
D015065:17-Hydroxycorticosteroids; D000001:Calcimycin; D011374:Progesterone; D014222:Triamcinolone Acetonide; D008274:Magnesium; D002118:Calcium; D003350:Cortodoxone; D014529:Uridine; D006854:Hydrocortisone