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Article: Regulation of voltage-gated cardiac sodium current by epidermal growth factor receptor kinase in guinea pig ventricular myocytes

TitleRegulation of voltage-gated cardiac sodium current by epidermal growth factor receptor kinase in guinea pig ventricular myocytes
Authors
Issue Date2007
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 2007, v. 42 n. 4, p. 760-768 How to Cite?
AbstractVoltage-gated cardiac fast sodium channel current (INa) plays a critical role in the initiation and propagation of the myocardial action potential, and regulation of cardiac INa by protein tyrosine kinases (PTKs) is not well documented, though it is known that ion channels are among the targets of PTKs. The present study was therefore designed to investigate whether/how cardiac INa was modulated by PTKs in guinea pig ventricular myocytes using whole-cell patch clamp and immunoprecipitation and Western blotting approaches. It was found that cardiac INa was enhanced by epidermal growth factor (EGF), and the effect was antagonized by the selective epidermal growth factor receptor (EGFR) kinase inhibitor tyrphostin AG556 while potentiated by orthovanadate (a protein tyrosine phosphatase (PTP) inhibitor). In addition, AG556 inhibited, while orthovanadate increased INa, and the inhibition of INa by AG556 was antagonized by orthovanadate. Immunoprecipitation and Western blotting analysis demonstrated that tyrosine phosphorylation level of cardiac sodium channels was enhanced by EGF or orthovanadate, and reduced by AG556. The AG556-induced reduction of phosphorylation level was significantly reversed by orthovanadate. Our results demonstrate the novel information that EGFR kinase enhances, and PTPs reduce native cardiac INa in guinea pig ventricular myocytes. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76561
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Hen_HK
dc.contributor.authorSun, HYen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2010-09-06T07:22:32Z-
dc.date.available2010-09-06T07:22:32Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 2007, v. 42 n. 4, p. 760-768en_HK
dc.identifier.issn0022-2828en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76561-
dc.description.abstractVoltage-gated cardiac fast sodium channel current (INa) plays a critical role in the initiation and propagation of the myocardial action potential, and regulation of cardiac INa by protein tyrosine kinases (PTKs) is not well documented, though it is known that ion channels are among the targets of PTKs. The present study was therefore designed to investigate whether/how cardiac INa was modulated by PTKs in guinea pig ventricular myocytes using whole-cell patch clamp and immunoprecipitation and Western blotting approaches. It was found that cardiac INa was enhanced by epidermal growth factor (EGF), and the effect was antagonized by the selective epidermal growth factor receptor (EGFR) kinase inhibitor tyrphostin AG556 while potentiated by orthovanadate (a protein tyrosine phosphatase (PTP) inhibitor). In addition, AG556 inhibited, while orthovanadate increased INa, and the inhibition of INa by AG556 was antagonized by orthovanadate. Immunoprecipitation and Western blotting analysis demonstrated that tyrosine phosphorylation level of cardiac sodium channels was enhanced by EGF or orthovanadate, and reduced by AG556. The AG556-induced reduction of phosphorylation level was significantly reversed by orthovanadate. Our results demonstrate the novel information that EGFR kinase enhances, and PTPs reduce native cardiac INa in guinea pig ventricular myocytes. © 2006 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_HK
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshElectrophysiologic Techniques, Cardiacen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGuinea Pigsen_HK
dc.subject.meshHeart Ventricles - cytology - drug effects - enzymologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMyocytes, Cardiac - drug effects - enzymologyen_HK
dc.subject.meshPhosphorylation - drug effectsen_HK
dc.subject.meshProtein Kinase Inhibitors - pharmacologyen_HK
dc.subject.meshReceptor, Epidermal Growth Factor - metabolismen_HK
dc.subject.meshSodium - metabolismen_HK
dc.subject.meshSodium Channels - drug effects - metabolismen_HK
dc.subject.meshTyrosine - metabolismen_HK
dc.titleRegulation of voltage-gated cardiac sodium current by epidermal growth factor receptor kinase in guinea pig ventricular myocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2828&volume=42&issue=4&spage=760&epage=8&date=2007&atitle=Regulation+of+voltage-gated+cardiac+sodium+current+by+epidermal+growth+factor+receptor+kinase+in+guinea+pig+ventricular+myocytes.++++en_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yjmcc.2006.10.013en_HK
dc.identifier.pmid17188293-
dc.identifier.scopuseid_2-s2.0-34047270735en_HK
dc.identifier.hkuros139374en_HK
dc.identifier.hkuros125285-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34047270735&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume42en_HK
dc.identifier.issue4en_HK
dc.identifier.spage760en_HK
dc.identifier.epage768en_HK
dc.identifier.isiWOS:000246287600009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLiu, H=27170235100en_HK
dc.identifier.scopusauthoridSun, HY=35723049200en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK

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