AI Article Synopsis
- The study investigates how the hormone 17β-estradiol affects TASK-1 expression in nerve cells (N2A), revealing potential neuroprotective effects.
- Knockdown experiments show that estrogen receptor β (ERβ) is the specific receptor that interacts with 17β-estradiol, rather than estrogen receptor α.
- The findings indicate that the neuroprotective actions of estrogen are likely mediated through ERβ, suggesting a role for TASK-1 channels in promoting cell proliferation.
Article 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.
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| http://dx.doi.org/10.1007/s11033-021-06852-6 | DOI Listing |
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