Predisposition to arrhythmia and autonomic dysfunction in Nhlh1-deficient mice

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dc.contributor.authorCogliati, Tizianaen
dc.contributor.authorGood, Deborah J.en
dc.contributor.authorHaigney, Marken
dc.contributor.authorDelgado-Romero, Petraen
dc.contributor.authorEckhaus, Michael A.en
dc.contributor.authorKoch, Walter J.en
dc.contributor.authorKirsch, Ilan R.en
dc.date.accessioned2025-01-03T13:28:22Zen
dc.date.available2025-01-03T13:28:22Zen
dc.date.issued2002-07en
dc.description.abstractNhlh1 is a basic helix-loop-helix transcription factor whose expression is restricted to the nervous system and which may play a role in neuronal differentiation. To directly study Nhlh1 function, we generated null mice. Homozygous mutant mice were predisposed to premature, adult-onset, unexpected death. Electrocardiograms revealed decreased total heart rate variability, stress-induced arrhythmia, and impaired baroreceptor sensitivity. This predisposition to arrhythmia is a likely cause of the observed death in the mutant mice. Heterozygosity for the closely related transcription factor Nhlh2 increased the severity of the Nhlh1-null phenotype. No signs of primary cardiac structural or conduction abnormalities could be detected upon necropsy of the null mice. The pattern of altered heart rhythm observed in basal and experimental conditions (stress and pharmacologically induced) suggests that a deficient parasympathetic tone may contribute to the arrhythmia in the Nhlh1-null mouse. The expression of Nhlh1 in the developing brain stem and in the vagal nuclei in the wild-type mouse further supports this hypothesis. The Nhlh1 mutant mouse may thus provide a model to investigate the contribution of the autonomic nervous system to arrhythmogenesis.en
dc.description.versionPublished versionen
dc.format.extentPages 4977-4983en
dc.format.extent7 page(s)en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1128/MCB.22.14.4977-4983.2002en
dc.identifier.eissn1098-5549en
dc.identifier.issn0270-7306en
dc.identifier.issue14en
dc.identifier.orcidGood, Deborah [0000-0003-0136-0975]en
dc.identifier.pmid12077327en
dc.identifier.urihttps://hdl.handle.net/10919/123886en
dc.identifier.volume22en
dc.language.isoenen
dc.publisherAmerican Society for Microbiologyen
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/12077327en
dc.rightsPublic Domain (U.S.)en
dc.rights.urihttp://creativecommons.org/publicdomain/mark/1.0/en
dc.subject.meshHeart Conduction Systemen
dc.subject.meshBrain Stemen
dc.subject.meshPressoreceptorsen
dc.subject.meshAnimalsen
dc.subject.meshMice, Knockouten
dc.subject.meshMiceen
dc.subject.meshAutonomic Nervous System Diseasesen
dc.subject.meshBradycardiaen
dc.subject.meshDisease Models, Animalen
dc.subject.meshDNA-Binding Proteinsen
dc.subject.meshElectrocardiographyen
dc.subject.meshIn Situ Hybridizationen
dc.subject.meshGene Targetingen
dc.subject.meshDivingen
dc.subject.meshGene Expression Regulation, Developmentalen
dc.subject.meshLongevityen
dc.subject.meshHeart Rateen
dc.subject.meshHeterozygoteen
dc.subject.meshHomozygoteen
dc.subject.meshPhenotypeen
dc.subject.meshBasic Helix-Loop-Helix Transcription Factorsen
dc.subject.meshArrhythmias, Cardiacen
dc.titlePredisposition to arrhythmia and autonomic dysfunction in <i>Nhlh1</i>-deficient miceen
dc.title.serialMolecular and Cellular Biologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherArticleen
dc.type.otherJournalen
pubs.organisational-groupVirginia Techen
pubs.organisational-groupVirginia Tech/Agriculture & Life Sciencesen
pubs.organisational-groupVirginia Tech/Agriculture & Life Sciences/Human Nutrition, Foods, & Exerciseen
pubs.organisational-groupVirginia Tech/Faculty of Health Sciencesen
pubs.organisational-groupVirginia Tech/All T&R Facultyen
pubs.organisational-groupVirginia Tech/Agriculture & Life Sciences/CALS T&R Facultyen

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