Abstract
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.
Keywords:
Estrogen; Estrogen receptor; N2A cells; TASK-1 channels.
© 2021. The Author(s), under exclusive licence to Springer Nature B.V.
MeSH terms
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Animals
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Cell Line
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Cell Proliferation / drug effects
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Cell Proliferation / genetics
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Down-Regulation / drug effects*
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Down-Regulation / genetics
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Estradiol / pharmacology*
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Estrogen Receptor alpha / genetics
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Estrogen Receptor alpha / metabolism
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Estrogen Receptor beta / genetics
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Estrogen Receptor beta / metabolism*
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Estrogens / pharmacology*
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Gene Knockdown Techniques / methods
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Mice
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism*
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Neural Crest / metabolism*
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Neuroprotective Agents / pharmacology*
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Polymerase Chain Reaction / methods
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Potassium Channels, Tandem Pore Domain / genetics
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Potassium Channels, Tandem Pore Domain / metabolism*
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RNA Interference
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RNA, Messenger / metabolism
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Signal Transduction / drug effects*
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Signal Transduction / genetics
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Transfection
Substances
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Estrogen Receptor alpha
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Estrogen Receptor beta
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Estrogens
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Nerve Tissue Proteins
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Neuroprotective Agents
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Potassium Channels, Tandem Pore Domain
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RNA, Messenger
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potassium channel subfamily K member 3
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Estradiol