Knockout of the neural and heart expressed gene HF-1b results in apical deficits of ventricular structure and activation

Knockout of the neural and cardiac expressed transcription factor HF-1b causes electrophysiological abnormalities including fatal ventricular arrhythmias that occur with increasing frequency around the 4th week of postnatal life. This study addresses factors that may contribute to conduction disturb...

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Bibliographic Details
Published in:Cardiovascular research 2005-08, Vol.67 (3), p.548-560
Main Authors: HEWETT, Kenneth W, NORMAN, Lisa W, SEDMERA, David, BARKER, Ralph J, JUSTUS, Charles, JING ZHANG, KUBALAK, Steven W, GOURDIE, Robert G
Format: Article
Language:English
Subjects:
Actins - analysis
Animals
Biological and medical sciences
Biomarkers - analysis
Blotting, Western - methods
Cardiac dysrhythmias
Cardiology. Vascular system
Cell Size
Connexin 43 - analysis
Coronary Vessels - metabolism
Coronary Vessels - pathology
Electrophysiology
Heart
Heart Conduction System
Heart Ventricles
Medical sciences
Mice
Mice, Knockout
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
Sp4 Transcription Factor - analysis
Sp4 Transcription Factor - genetics
Ventricular Fibrillation - genetics
Ventricular Fibrillation - metabolism
Ventricular Fibrillation - pathology
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Summary:Knockout of the neural and cardiac expressed transcription factor HF-1b causes electrophysiological abnormalities including fatal ventricular arrhythmias that occur with increasing frequency around the 4th week of postnatal life. This study addresses factors that may contribute to conduction disturbance in the ventricle of the HF-1b knockout mouse. Disruptions to gap junctional connexin40 (Cx40) have been reported in distal (i.e., apically located), but not proximal His-Purkinje conduction tissues of the HF-1b knockout mouse. This abnormality in myocardial Cx40 led us to address whether 4-week-old HF-1b knockout postnates display other disruptions to ventricular structure and function. Western blotting and immunoconfocal quantification of Cx43 and coronary arteriole density and function were undertaken in the ventricle. Electrical activation was described by optical mapping. Western blotting and immunoconfocal microscopy indicated that overall levels of Cx43 (p
ISSN:0008-6363
1755-3245
DOI:10.1016/j.cardiores.2005.04.002