Rapid effects of 17beta-estradiol on TRPV5 epithelial Ca2+ channels in rat renal cells.

Hdl Handle:
http://hdl.handle.net/10147/127508
Title:
Rapid effects of 17beta-estradiol on TRPV5 epithelial Ca2+ channels in rat renal cells.
Authors:
Irnaten, Mustapha; Blanchard-Gutton, Nicolas; Praetorius, Jeppe; Harvey, Brian J
Affiliation:
Molecular Medicine Laboratories, Royal College of Surgeons in Ireland, Beaumont Hospital, PO Box 9063, Dublin 9, Ireland. irnatenm@yahoo.fr
Citation:
Rapid effects of 17beta-estradiol on TRPV5 epithelial Ca2+ channels in rat renal cells. 2009, 74 (8):642-9 Steroids
Journal:
Steroids
Issue Date:
Aug-2009
URI:
http://hdl.handle.net/10147/127508
DOI:
10.1016/j.steroids.2009.02.002
PubMed ID:
19463684
Abstract:
The renal distal tubules and collecting ducts play a key role in the control of electrolyte and fluid homeostasis. The discovery of highly calcium selective channels, Transient Receptor Potential Vanilloid 5 (TRPV5) of the TRP superfamily, has clarified the nature of the calcium entry channels. It has been proposed that this channel mediates the critical Ca(2+) entry step in transcellular Ca(2+) re-absorption in the kidney. The regulation of transmembrane Ca(2+) flux through TRPV5 is of particular importance for whole body calcium homeostasis.In this study, we provide evidence that the TRPV5 channel is present in rat cortical collecting duct (RCCD(2)) cells at mRNA and protein levels. We demonstrate that 17beta-estradiol (E(2)) is involved in the regulation of Ca(2+) influx in these cells via the epithelial Ca(2+) channels TRPV5. By combining whole-cell patch-clamp and Ca(2+)-imaging techniques, we have characterized the electrophysiological properties of the TRPV5 channel and showed that treatment with 20-50nM E(2) rapidly (<5min) induced a transient increase in inward whole-cell currents and intracellular Ca(2+) via TRPV5 channels. This rise was significantly prevented when cells were pre-treated with ruthenium red and completely abolished in cells treated with siRNA specifically targeting TRPV5.These data demonstrate for the first time, a novel rapid modulation of endogenously expressed TRPV5 channels by E(2) in kidney cells. Furthermore, the results suggest calcitropic effects of E(2). The results are discussed in relation to present concepts of non-genomic actions of E(2) in Ca(2+) homeostasis.
Item Type:
Article
Language:
en
MeSH:
Animals; Calcium; Calcium Channels; Cell Line; Electrophysiological Processes; Estradiol; Gene Expression Regulation; Gene Knockdown Techniques; Intracellular Space; Kidney; Male; Patch-Clamp Techniques; RNA, Small Interfering; Rats; Ruthenium Red; TRPV Cation Channels; Time Factors
ISSN:
1878-5867

Full metadata record

DC FieldValue Language
dc.contributor.authorIrnaten, Mustaphaen
dc.contributor.authorBlanchard-Gutton, Nicolasen
dc.contributor.authorPraetorius, Jeppeen
dc.contributor.authorHarvey, Brian Jen
dc.date.accessioned2011-04-06T14:58:19Z-
dc.date.available2011-04-06T14:58:19Z-
dc.date.issued2009-08-
dc.identifier.citationRapid effects of 17beta-estradiol on TRPV5 epithelial Ca2+ channels in rat renal cells. 2009, 74 (8):642-9 Steroidsen
dc.identifier.issn1878-5867-
dc.identifier.pmid19463684-
dc.identifier.doi10.1016/j.steroids.2009.02.002-
dc.identifier.urihttp://hdl.handle.net/10147/127508-
dc.description.abstractThe renal distal tubules and collecting ducts play a key role in the control of electrolyte and fluid homeostasis. The discovery of highly calcium selective channels, Transient Receptor Potential Vanilloid 5 (TRPV5) of the TRP superfamily, has clarified the nature of the calcium entry channels. It has been proposed that this channel mediates the critical Ca(2+) entry step in transcellular Ca(2+) re-absorption in the kidney. The regulation of transmembrane Ca(2+) flux through TRPV5 is of particular importance for whole body calcium homeostasis.In this study, we provide evidence that the TRPV5 channel is present in rat cortical collecting duct (RCCD(2)) cells at mRNA and protein levels. We demonstrate that 17beta-estradiol (E(2)) is involved in the regulation of Ca(2+) influx in these cells via the epithelial Ca(2+) channels TRPV5. By combining whole-cell patch-clamp and Ca(2+)-imaging techniques, we have characterized the electrophysiological properties of the TRPV5 channel and showed that treatment with 20-50nM E(2) rapidly (<5min) induced a transient increase in inward whole-cell currents and intracellular Ca(2+) via TRPV5 channels. This rise was significantly prevented when cells were pre-treated with ruthenium red and completely abolished in cells treated with siRNA specifically targeting TRPV5.These data demonstrate for the first time, a novel rapid modulation of endogenously expressed TRPV5 channels by E(2) in kidney cells. Furthermore, the results suggest calcitropic effects of E(2). The results are discussed in relation to present concepts of non-genomic actions of E(2) in Ca(2+) homeostasis.-
dc.language.isoenen
dc.subject.meshAnimals-
dc.subject.meshCalcium-
dc.subject.meshCalcium Channels-
dc.subject.meshCell Line-
dc.subject.meshElectrophysiological Processes-
dc.subject.meshEstradiol-
dc.subject.meshGene Expression Regulation-
dc.subject.meshGene Knockdown Techniques-
dc.subject.meshIntracellular Space-
dc.subject.meshKidney-
dc.subject.meshMale-
dc.subject.meshPatch-Clamp Techniques-
dc.subject.meshRNA, Small Interfering-
dc.subject.meshRats-
dc.subject.meshRuthenium Red-
dc.subject.meshTRPV Cation Channels-
dc.subject.meshTime Factors-
dc.titleRapid effects of 17beta-estradiol on TRPV5 epithelial Ca2+ channels in rat renal cells.en
dc.typeArticleen
dc.contributor.departmentMolecular Medicine Laboratories, Royal College of Surgeons in Ireland, Beaumont Hospital, PO Box 9063, Dublin 9, Ireland. irnatenm@yahoo.fren
dc.identifier.journalSteroidsen
dc.description.provinceLeinster-

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