Abstract
We recently reported that physiological concentrations of 17beta-estradiol partially down-regulate cardiac rapidly-activating delayed rectifier K(+) currents (hERG currents) independently of estrogen-receptor signaling. To determine if other estrogens have the same effect as that of 17beta-estradiol, we investigated receptor-independent effects of estrone, estrone 3-sulfate, and estriol on hERG currents in patch-clamped estrogen-negative HEK293 cells. Only estrone 3-sulfate partially suppressed hERG currents in a receptor-independent manner by modifying the gating. The concentration-dependence of estrone 3-sulfate revealed that physiological levels of circulating estrone 3-sulfate can modulate hERG currents to the maximal extent in both women and men at any age.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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Dose-Response Relationship, Drug
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ERG1 Potassium Channel
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Estradiol / pharmacology
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Estrogen Antagonists / pharmacology
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Estrogens / chemistry
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Estrogens / pharmacology
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Estrone / analogs & derivatives*
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Estrone / chemistry
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Estrone / pharmacology
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Ether-A-Go-Go Potassium Channels / genetics
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Ether-A-Go-Go Potassium Channels / physiology*
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Gene Expression
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Humans
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Molecular Structure
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Patch-Clamp Techniques
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Receptors, Estrogen / antagonists & inhibitors
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Receptors, Estrogen / physiology*
Substances
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ERG1 Potassium Channel
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Estrogen Antagonists
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Estrogens
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Ether-A-Go-Go Potassium Channels
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KCNH2 protein, human
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Receptors, Estrogen
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Estrone
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Estradiol
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estrone sulfate