Estradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells.

Hdl Handle:
http://hdl.handle.net/10147/127674
Title:
Estradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells.
Authors:
Muchekehu, Ruth W; Harvey, Brian J
Affiliation:
Molecular Medicine Laboratories, Royal College of Surgeons in Ireland, RCSI Education and Research Centre, Smurfit Building, Beaumont Hospital, P.O. Box 9063, Dublin 9, Ireland. rmuchekehu@ucsd.edu
Citation:
Estradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells. 2009, 74 (2):212-7 Steroids
Journal:
Steroids
Issue Date:
Feb-2009
URI:
http://hdl.handle.net/10147/127674
DOI:
10.1016/j.steroids.2008.10.013
PubMed ID:
19027769
Abstract:
Steroid hormones target K+ channels as a means of regulating electrolyte and fluid transport. In this study, ion transporter targets of Estradiol (E2) were investigated in the human eccrine sweat gland cell line NCL-SG3.; Whole cell patch-clamp studies revealed E2 (10 nM) rapidly activates a whole cell K+ conductance, which is abolished by clotrimazole (30 microM), an inhibitor of the intermediate conductance calcium activated K+ channel (IKCa). The estrogen receptor (ER) antagonist ICI 182, 780 had no effect on this E2 activated K+ conductance, suggesting an estrogen receptor independent mechanism of activation. Confocal microscopy studies revealed under basal conditions that the IKCa channel is located within the cell cytoplasm and in the presence of E2, rapidly translocates to both the apical and basolateral membrane. In the presence of E2, tyrosine phosphorylation of calmodulin, which is known to regulate trafficking of the IKCa channel, is increased, and treatment of cells with the calmodulin inhibitor trifluoperazine (TFP) prevents the E2-induced translocation.; Estradiol rapidly regulates a K+ conductance through the IKCa channel in an estrogen receptor independent manner. E2 stimulates the translocation of IKCa to the cell membrane in a calmodulin dependent manner, representing a novel paradigm of estrogen action in sweat gland epithelial cells.
Item Type:
Article
Language:
en
MeSH:
Calmodulin; Cell Line; Cell Membrane; Eccrine Glands; Electric Conductivity; Epithelial Cells; Estradiol; Humans; Phosphorylation; Potassium Channels, Calcium-Activated; Protein Transport; Receptors, Estrogen; Time Factors; Tyrosine
ISSN:
0039-128X

Full metadata record

DC FieldValue Language
dc.contributor.authorMuchekehu, Ruth Wen
dc.contributor.authorHarvey, Brian Jen
dc.date.accessioned2011-04-07T10:45:17Z-
dc.date.available2011-04-07T10:45:17Z-
dc.date.issued2009-02-
dc.identifier.citationEstradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells. 2009, 74 (2):212-7 Steroidsen
dc.identifier.issn0039-128X-
dc.identifier.pmid19027769-
dc.identifier.doi10.1016/j.steroids.2008.10.013-
dc.identifier.urihttp://hdl.handle.net/10147/127674-
dc.description.abstractSteroid hormones target K+ channels as a means of regulating electrolyte and fluid transport. In this study, ion transporter targets of Estradiol (E2) were investigated in the human eccrine sweat gland cell line NCL-SG3.-
dc.description.abstractWhole cell patch-clamp studies revealed E2 (10 nM) rapidly activates a whole cell K+ conductance, which is abolished by clotrimazole (30 microM), an inhibitor of the intermediate conductance calcium activated K+ channel (IKCa). The estrogen receptor (ER) antagonist ICI 182, 780 had no effect on this E2 activated K+ conductance, suggesting an estrogen receptor independent mechanism of activation. Confocal microscopy studies revealed under basal conditions that the IKCa channel is located within the cell cytoplasm and in the presence of E2, rapidly translocates to both the apical and basolateral membrane. In the presence of E2, tyrosine phosphorylation of calmodulin, which is known to regulate trafficking of the IKCa channel, is increased, and treatment of cells with the calmodulin inhibitor trifluoperazine (TFP) prevents the E2-induced translocation.-
dc.description.abstractEstradiol rapidly regulates a K+ conductance through the IKCa channel in an estrogen receptor independent manner. E2 stimulates the translocation of IKCa to the cell membrane in a calmodulin dependent manner, representing a novel paradigm of estrogen action in sweat gland epithelial cells.-
dc.language.isoenen
dc.subject.meshCalmodulin-
dc.subject.meshCell Line-
dc.subject.meshCell Membrane-
dc.subject.meshEccrine Glands-
dc.subject.meshElectric Conductivity-
dc.subject.meshEpithelial Cells-
dc.subject.meshEstradiol-
dc.subject.meshHumans-
dc.subject.meshPhosphorylation-
dc.subject.meshPotassium Channels, Calcium-Activated-
dc.subject.meshProtein Transport-
dc.subject.meshReceptors, Estrogen-
dc.subject.meshTime Factors-
dc.subject.meshTyrosine-
dc.titleEstradiol rapidly induces the translocation and activation of the intermediate conductance calcium activated potassium channel in human eccrine sweat gland cells.en
dc.typeArticleen
dc.contributor.departmentMolecular Medicine Laboratories, Royal College of Surgeons in Ireland, RCSI Education and Research Centre, Smurfit Building, Beaumont Hospital, P.O. Box 9063, Dublin 9, Ireland. rmuchekehu@ucsd.eduen
dc.identifier.journalSteroidsen
dc.description.provinceLeinster-
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