The thymolytic action of dexamethasone (DEXA) and aldosterone (ALDO) has been studied in vitro and in vivo. In vitro, in the presence of DEXA, the number of apoptotic cells increased with time. After 6 hours of incubation, 55 and 86% of thymocytes are dead with 10(-7) and 10(-5) M of DEXA, respectively. Whereas, in the presence of equivalent concentrations of ALDO, the rate of mortality of cells was only 30-40%. In vivo study confirmed these results and showed that apoptotic action of ALDO remained less potent than that of DEXA. On the other hand, addition of the potent glucocorticoid antagonist, RU 38486 prevents not only the dexamethasone but also the aldosterone-stimulated cell death. We conclude that the thymolytic action of the endogenous mineralocorticoid hormone is not mediated by its specific receptor but paradoxically by type II glucocorticoid receptor.
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