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Article: Antiarrhythmic engineering of skeletal myoblasts for cardiac transplantation

TitleAntiarrhythmic engineering of skeletal myoblasts for cardiac transplantation
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2005
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 2005, v. 97 n. 2, p. 159-167 How to Cite?
AbstractSkeletal myoblasts are an attractive cell type for transplantation because they are autologous and resistant to ischemia. However, clinical trials of myoblast transplantation in heart failure have been plagued by ventricular tachyarrhythmias and sudden cardiac death. The pathogenesis of these arrhythmias is poorly understood, but may be related to the fact that skeletal muscle cells, unlike heart cells, are electrically isolated by the absence of gap junctions. Using a novel in vitro model of myoblast transplantation in cardiomyocyte monolayers, we investigated the mechanisms of transplant- associated arrhythmias. Cocultures of human skeletal myoblasts and rat cardiomyocytes resulted in reentrant arrhythmias (spiral waves) that reproduce the features of ventricular tachycardia seen in patients receiving myoblast transplants. These arrhythmias could be terminated by nitrendipine, an L-type calcium channel blocker, but not by the Na channel blocker lidocaine. Genetic modification of myoblasts to express the gap junction protein connexin43 decreased arrhythmogenicity in cocultures, suggesting a specific means for increasing the safety (and perhaps the efficacy) of myoblast transplantation in patients. © 2005 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/91595
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAbraham, MRen_HK
dc.contributor.authorHenrikson, CAen_HK
dc.contributor.authorTung, Len_HK
dc.contributor.authorChang, MGen_HK
dc.contributor.authorAon, Men_HK
dc.contributor.authorXue, Ten_HK
dc.contributor.authorLi, RAen_HK
dc.contributor.authorO'Rourke, Ben_HK
dc.contributor.authorMarbán, Een_HK
dc.date.accessioned2010-09-17T10:21:56Z-
dc.date.available2010-09-17T10:21:56Z-
dc.date.issued2005en_HK
dc.identifier.citationCirculation Research, 2005, v. 97 n. 2, p. 159-167en_HK
dc.identifier.issn0009-7330en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91595-
dc.description.abstractSkeletal myoblasts are an attractive cell type for transplantation because they are autologous and resistant to ischemia. However, clinical trials of myoblast transplantation in heart failure have been plagued by ventricular tachyarrhythmias and sudden cardiac death. The pathogenesis of these arrhythmias is poorly understood, but may be related to the fact that skeletal muscle cells, unlike heart cells, are electrically isolated by the absence of gap junctions. Using a novel in vitro model of myoblast transplantation in cardiomyocyte monolayers, we investigated the mechanisms of transplant- associated arrhythmias. Cocultures of human skeletal myoblasts and rat cardiomyocytes resulted in reentrant arrhythmias (spiral waves) that reproduce the features of ventricular tachycardia seen in patients receiving myoblast transplants. These arrhythmias could be terminated by nitrendipine, an L-type calcium channel blocker, but not by the Na channel blocker lidocaine. Genetic modification of myoblasts to express the gap junction protein connexin43 decreased arrhythmogenicity in cocultures, suggesting a specific means for increasing the safety (and perhaps the efficacy) of myoblast transplantation in patients. © 2005 American Heart Association, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_HK
dc.relation.ispartofCirculation Researchen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshAction Potentialsen_HK
dc.subject.meshArrhythmias, Cardiac - etiology - prevention & controlen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCoculture Techniquesen_HK
dc.subject.meshConnexin 43 - genetics - physiologyen_HK
dc.subject.meshGene Therapyen_HK
dc.subject.meshHeLa Cellsen_HK
dc.subject.meshHeart Transplantation - adverse effectsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMuscle Fibers, Skeletal - physiologyen_HK
dc.subject.meshMuscle, Skeletal - embryologyen_HK
dc.subject.meshMyoblasts - physiology - transplantationen_HK
dc.titleAntiarrhythmic engineering of skeletal myoblasts for cardiac transplantationen_HK
dc.typeArticleen_HK
dc.identifier.emailLi, RA:ronaldli@hkucc.hku.hken_HK
dc.identifier.authorityLi, RA=rp01352en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1161/01.RES.0000174794.22491.a0en_HK
dc.identifier.pmid15976318en_HK
dc.identifier.scopuseid_2-s2.0-22744447315en_HK
dc.identifier.hkuros183066-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-22744447315&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue2en_HK
dc.identifier.spage159en_HK
dc.identifier.epage167en_HK
dc.identifier.isiWOS:000230668900010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridAbraham, MR=7202901126en_HK
dc.identifier.scopusauthoridHenrikson, CA=7004279066en_HK
dc.identifier.scopusauthoridTung, L=7102531482en_HK
dc.identifier.scopusauthoridChang, MG=8536811500en_HK
dc.identifier.scopusauthoridAon, M=7003963839en_HK
dc.identifier.scopusauthoridXue, T=7005064190en_HK
dc.identifier.scopusauthoridLi, RA=7404724466en_HK
dc.identifier.scopusauthoridO'Rourke, B=7006763781en_HK
dc.identifier.scopusauthoridMarbán, E=8075977300en_HK
dc.identifier.citeulike880028-
dc.customcontrol.immutablesml 140917-

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