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Article: Cyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure

TitleCyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure
Authors
Issue Date2007
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 2007, v. 100 n. 12, p. 1741-1748 How to Cite?
AbstractMammalian myocardial infarction is typically followed by scar formation with eventual ventricular dilation and heart failure. Here we present a novel model system in which mice constitutively expressing cyclin A2 in the myocardium elicit a regenerative response after infarction and exhibit significantly limited ventricular dilation with sustained and remarkably enhanced cardiac function. New cardiomyocyte formation was noted in the infarcted zones as well as cell cycle reentry of periinfarct myocardium with an increase in DNA synthesis and mitotic indices. The enhanced cardiac function was serially assessed over time by MRI. Furthermore, the constitutive expression of cyclin A2 appears to augment endogenous regenerative mechanisms via induction of side population cells with enhanced proliferative capacity. The ability of cultured transgenic cardiomyocytes to undergo cytokinesis provides mechanistic support for the regenerative capacity of cyclin A2. © 2007 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/155378
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, RKen_US
dc.contributor.authorAsai, Ten_US
dc.contributor.authorTang, Hen_US
dc.contributor.authorDashoush, NHen_US
dc.contributor.authorKara, RJen_US
dc.contributor.authorCosta, KDen_US
dc.contributor.authorNaka, Yen_US
dc.contributor.authorWu, EXen_US
dc.contributor.authorWolgemuth, DJen_US
dc.contributor.authorChaudhry, HWen_US
dc.date.accessioned2012-08-08T08:33:09Z-
dc.date.available2012-08-08T08:33:09Z-
dc.date.issued2007en_US
dc.identifier.citationCirculation Research, 2007, v. 100 n. 12, p. 1741-1748en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/155378-
dc.description.abstractMammalian myocardial infarction is typically followed by scar formation with eventual ventricular dilation and heart failure. Here we present a novel model system in which mice constitutively expressing cyclin A2 in the myocardium elicit a regenerative response after infarction and exhibit significantly limited ventricular dilation with sustained and remarkably enhanced cardiac function. New cardiomyocyte formation was noted in the infarcted zones as well as cell cycle reentry of periinfarct myocardium with an increase in DNA synthesis and mitotic indices. The enhanced cardiac function was serially assessed over time by MRI. Furthermore, the constitutive expression of cyclin A2 appears to augment endogenous regenerative mechanisms via induction of side population cells with enhanced proliferative capacity. The ability of cultured transgenic cardiomyocytes to undergo cytokinesis provides mechanistic support for the regenerative capacity of cyclin A2. © 2007 American Heart Association, Inc.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.rightsCirculation Research. Copyright © Lippincott Williams & Wilkins.-
dc.subject.meshAnimalsen_US
dc.subject.meshCardiac Output, Low - Physiopathology - Prevention & Controlen_US
dc.subject.meshCell Cycle - Physiologyen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclin A - Genetics - Physiologyen_US
dc.subject.meshCyclin A2en_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshHeart - Physiologyen_US
dc.subject.meshMagnetic Resonance Imagingen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshMitotic Indexen_US
dc.subject.meshMyocardial Infarction - Pathology - Physiopathologyen_US
dc.subject.meshMyocardium - Pathologyen_US
dc.subject.meshMyocytes, Cardiac - Pathology - Physiologyen_US
dc.subject.meshRegeneration - Physiologyen_US
dc.subject.meshStem Cells - Physiologyen_US
dc.titleCyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failureen_US
dc.typeArticleen_US
dc.identifier.emailWu, EX:ewu1@hkucc.hku.hken_US
dc.identifier.authorityWu, EX=rp00193en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1161/CIRCRESAHA.107.153544en_US
dc.identifier.pmid17495221-
dc.identifier.scopuseid_2-s2.0-34250857995en_US
dc.identifier.hkuros134605-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34250857995&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume100en_US
dc.identifier.issue12en_US
dc.identifier.spage1741en_US
dc.identifier.epage1748en_US
dc.identifier.isiWOS:000247530800010-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCheng, RK=7201955298en_US
dc.identifier.scopusauthoridAsai, T=55127277400en_US
dc.identifier.scopusauthoridTang, H=36827331000en_US
dc.identifier.scopusauthoridDashoush, NH=6504551155en_US
dc.identifier.scopusauthoridKara, RJ=16175598800en_US
dc.identifier.scopusauthoridCosta, KD=26638724700en_US
dc.identifier.scopusauthoridNaka, Y=7103397000en_US
dc.identifier.scopusauthoridWu, EX=7202128034en_US
dc.identifier.scopusauthoridWolgemuth, DJ=7102345248en_US
dc.identifier.scopusauthoridChaudhry, HW=14065840300en_US

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