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Article: Evidence for cystic fibrosis transmembrane conductance regulator chloride current in swine ventricular myocytes

TitleEvidence for cystic fibrosis transmembrane conductance regulator chloride current in swine 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. 1, p. 98-105 How to Cite?
AbstractThe present study investigated whether cAMP-dependent cystic fibrosis transmembrane conductance regulator (CFTR) Cl - channel current (i.e., I Cl.CFTR or I Cl.cAMP) would be expressed in pig cardiac myocytes using whole-cell patch technique and reverse transcription polymerase chain reaction (RT-PCR). It was found that the β-adrenoceptor agonist isoproterenol activated a time-independent current in myocytes from the ventricle, but not the atrium of pig heart. Histamine and forskolin (an adenylate cyclase activator) induced a similar current in pig ventricular cells. The current induced by isoproterenol was blocked by the PKA inhibitor H-7, reduced by the replacement of external Cl - ion, and inhibited by the application of 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), but not 4′-diisothiocynatostilbene-2,2′-disulfonic acid (DIDS), typical of I Cl.CFTR. I Cl.CFTR showed a small difference in regional myocytes across the left ventricular wall from epicardium to endocardium. Isoproterenol-induced current was 3.1 ± 0.2 (n = 33), 2.8 ± 0.2 (n = 25) and 2.3 ± 0.2 pA/pF (n = 31) respectively in subepicardial, midmyocardial, and subendocardial myocytes (P < 0.05, subepicardium vs. subendocardium). RT-PCR and Western blotting analysis revealed that significant differences in CFTR channel mRNA and protein levels were present in atrial and ventricular cells, but not in regional ventricular cells across the ventricular wall from subepicardium to subendocardium. These results indicate that the functional CFTR channel (i.e., I Cl.CFTR) is present in ventricular myocytes, but not in atrial cells of pig heart. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/85502
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGao, Zen_HK
dc.contributor.authorSun, HYen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorChinWan Fung, Pen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2010-09-06T09:05:50Z-
dc.date.available2010-09-06T09:05:50Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 2007, v. 42 n. 1, p. 98-105en_HK
dc.identifier.issn0022-2828en_HK
dc.identifier.urihttp://hdl.handle.net/10722/85502-
dc.description.abstractThe present study investigated whether cAMP-dependent cystic fibrosis transmembrane conductance regulator (CFTR) Cl - channel current (i.e., I Cl.CFTR or I Cl.cAMP) would be expressed in pig cardiac myocytes using whole-cell patch technique and reverse transcription polymerase chain reaction (RT-PCR). It was found that the β-adrenoceptor agonist isoproterenol activated a time-independent current in myocytes from the ventricle, but not the atrium of pig heart. Histamine and forskolin (an adenylate cyclase activator) induced a similar current in pig ventricular cells. The current induced by isoproterenol was blocked by the PKA inhibitor H-7, reduced by the replacement of external Cl - ion, and inhibited by the application of 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), but not 4′-diisothiocynatostilbene-2,2′-disulfonic acid (DIDS), typical of I Cl.CFTR. I Cl.CFTR showed a small difference in regional myocytes across the left ventricular wall from epicardium to endocardium. Isoproterenol-induced current was 3.1 ± 0.2 (n = 33), 2.8 ± 0.2 (n = 25) and 2.3 ± 0.2 pA/pF (n = 31) respectively in subepicardial, midmyocardial, and subendocardial myocytes (P < 0.05, subepicardium vs. subendocardium). RT-PCR and Western blotting analysis revealed that significant differences in CFTR channel mRNA and protein levels were present in atrial and ventricular cells, but not in regional ventricular cells across the ventricular wall from subepicardium to subendocardium. These results indicate that the functional CFTR channel (i.e., I Cl.CFTR) is present in ventricular myocytes, but not in atrial cells of pig heart. © 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.mesh4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCystic Fibrosis Transmembrane Conductance Regulator - genetics - metabolismen_HK
dc.subject.meshDNA Primers - geneticsen_HK
dc.subject.meshEndocardium - cytology - metabolismen_HK
dc.subject.meshHeart Atria - cytology - metabolismen_HK
dc.subject.meshHeart Ventricles - cytology - metabolismen_HK
dc.subject.meshIsoproterenol - pharmacologyen_HK
dc.subject.meshMembrane Potentials - drug effectsen_HK
dc.subject.meshMyocardium - cytology - metabolismen_HK
dc.subject.meshMyocytes, Cardiac - drug effects - metabolismen_HK
dc.subject.meshPericardium - cytology - metabolismen_HK
dc.subject.meshRNA, Messenger - genetics - metabolismen_HK
dc.subject.meshSwineen_HK
dc.subject.meshTissue Distributionen_HK
dc.titleEvidence for cystic fibrosis transmembrane conductance regulator chloride current in swine ventricular myocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2828&volume=42&issue=1&spage=98&epage=105&date=2007&atitle=Evidence+for+cystic+fibrosis+transmembrane+conductance+regulator+chloride+current+in+swine+ventricular+myocytesen_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.2006.10.002en_HK
dc.identifier.pmid17112538-
dc.identifier.scopuseid_2-s2.0-33845743367en_HK
dc.identifier.hkuros125283en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845743367&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume42en_HK
dc.identifier.issue1en_HK
dc.identifier.spage98en_HK
dc.identifier.epage105en_HK
dc.identifier.isiWOS:000243617100011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridGao, Z=16549711200en_HK
dc.identifier.scopusauthoridSun, HY=35723049200en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridChinWan Fung, P=6504642578en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK

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