Estrogen-induced downregulation of TASK-1 expression through estrogen receptor ß in N2A cells.

BACKGROUND: Our previous data revealed that reduction of TASK-1 expression, as a consequence of exposure to 17ß-estradiol, could participate in neuroprotective effects in N2A cells. However, it is unclear which estrogen receptor underlies these effects of 17ß-estradiol. METHODS AND RESULTS: In this study, the knockdown experiments are carried out to clarify the estrogen receptor responsible for effects of estrogen on TASK-1 channels. Subsequently, data from QPCR measurements reveal that estrogen receptor ß (ERß), but not estrogen receptor α, serves as a binding target for 17ß-estradiol after a 48-h treatment. CONCLUSIONS: The current result suggests the implication of the ERß-dependent manner in the pro-proliferative action of estrogen via TASK-1 channels.