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

Background Our previous data revealed that reduction of TASK-1 expression, as a consequence of exposure to 17β-estradiol, could participate in neuroprotective effects in N2A cells. However, it is unclear which estrogen receptor underlies these effects of 17β-estradiol. Methods and results In this st...

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Bibliographic Details
Published in:Molecular biology reports 2022, Vol.49 (1), p.817-819
Main Authors: Qiu, Xiao-Yue, Li, Xian-Tao
Format: Article
Language:English
Subjects:
17β-Estradiol
Animal Anatomy
Animal Biochemistry
Biomedical and Life Sciences
Estrogen receptors
Estrogens
Histology
Life Sciences
Morphology
Neuroprotection
Potassium channels
Short Communication
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Summary:Background Our previous data revealed that reduction of TASK-1 expression, as a consequence of exposure to 17β-estradiol, could participate in neuroprotective effects in N2A cells. However, it is unclear which estrogen receptor underlies these effects of 17β-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 β (ERβ), but not estrogen receptor α, serves as a binding target for 17β-estradiol after a 48-h treatment. Conclusions The current result suggests the implication of the ERβ-dependent manner in the pro-proliferative action of estrogen via TASK-1 channels.
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-021-06852-6