Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle

The neuregulin receptor tyrosine kinase Erb-b4, initially linked to early cardiac development, is shown here to play a critical role in adult cardiac function. In wild-type mice, Erb-b4 protein localized to Z lines and to intercalated disks, suggesting a role in subcellular and intercellular communi...

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Publicado: 2005
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03636135_v289_n358-3_pH1153_GarciaRivello
http://hdl.handle.net/20.500.12110/paper_03636135_v289_n358-3_pH1153_GarciaRivello
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spelling paper:paper_03636135_v289_n358-3_pH1153_GarciaRivello2023-06-08T15:35:28Z Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle Conditional knockout erb-b2 Heart Mouse Neuregulin actin atrial natriuretic factor brain natriuretic peptide cre recombinase epidermal growth factor receptor 4 indo 1 myosin light chain animal experiment animal model animal tissue article cell communication cellular distribution congestive cardiomyopathy controlled study electrocardiography female gene inactivation gene targeting heart development heart muscle cell heart muscle contractility heart ventricle hypertrophy heterozygosity histochemistry immunofluorescence knockout mouse mouse nick end labeling nonhuman priority journal reverse transcription polymerase chain reaction Western blotting wild type Animals Cardiomegaly Cardiomyopathy, Dilated Disease Models, Animal Female Male Mice Mice, Inbred C57BL Mice, Knockout Myocardial Contraction Myocardium Receptor, Epidermal Growth Factor Signal Transduction The neuregulin receptor tyrosine kinase Erb-b4, initially linked to early cardiac development, is shown here to play a critical role in adult cardiac function. In wild-type mice, Erb-b4 protein localized to Z lines and to intercalated disks, suggesting a role in subcellular and intercellular communications of cardiomyocytes. Conditional inactivation of erb-b4 in ventricular muscle cells led to a severe dilated cardiomyopathy, characterized by thinned ventricular walls with eccentric hypertrophy, reduced contractility, and delayed conduction. This cardiac dysfunction may account for premature death in adult erb-b4-knockout mice. This study establishes a critical role for Erb-b4 in the maintenance of normal postnatal cardiac structure and function. Copyright © 2005 the American Physiological Society. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03636135_v289_n358-3_pH1153_GarciaRivello http://hdl.handle.net/20.500.12110/paper_03636135_v289_n358-3_pH1153_GarciaRivello
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Conditional knockout
erb-b2
Heart
Mouse
Neuregulin
actin
atrial natriuretic factor
brain natriuretic peptide
cre recombinase
epidermal growth factor receptor 4
indo 1
myosin light chain
animal experiment
animal model
animal tissue
article
cell communication
cellular distribution
congestive cardiomyopathy
controlled study
electrocardiography
female
gene inactivation
gene targeting
heart development
heart muscle cell
heart muscle contractility
heart ventricle hypertrophy
heterozygosity
histochemistry
immunofluorescence
knockout mouse
mouse
nick end labeling
nonhuman
priority journal
reverse transcription polymerase chain reaction
Western blotting
wild type
Animals
Cardiomegaly
Cardiomyopathy, Dilated
Disease Models, Animal
Female
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction
Myocardium
Receptor, Epidermal Growth Factor
Signal Transduction
spellingShingle Conditional knockout
erb-b2
Heart
Mouse
Neuregulin
actin
atrial natriuretic factor
brain natriuretic peptide
cre recombinase
epidermal growth factor receptor 4
indo 1
myosin light chain
animal experiment
animal model
animal tissue
article
cell communication
cellular distribution
congestive cardiomyopathy
controlled study
electrocardiography
female
gene inactivation
gene targeting
heart development
heart muscle cell
heart muscle contractility
heart ventricle hypertrophy
heterozygosity
histochemistry
immunofluorescence
knockout mouse
mouse
nick end labeling
nonhuman
priority journal
reverse transcription polymerase chain reaction
Western blotting
wild type
Animals
Cardiomegaly
Cardiomyopathy, Dilated
Disease Models, Animal
Female
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction
Myocardium
Receptor, Epidermal Growth Factor
Signal Transduction
Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle
topic_facet Conditional knockout
erb-b2
Heart
Mouse
Neuregulin
actin
atrial natriuretic factor
brain natriuretic peptide
cre recombinase
epidermal growth factor receptor 4
indo 1
myosin light chain
animal experiment
animal model
animal tissue
article
cell communication
cellular distribution
congestive cardiomyopathy
controlled study
electrocardiography
female
gene inactivation
gene targeting
heart development
heart muscle cell
heart muscle contractility
heart ventricle hypertrophy
heterozygosity
histochemistry
immunofluorescence
knockout mouse
mouse
nick end labeling
nonhuman
priority journal
reverse transcription polymerase chain reaction
Western blotting
wild type
Animals
Cardiomegaly
Cardiomyopathy, Dilated
Disease Models, Animal
Female
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction
Myocardium
Receptor, Epidermal Growth Factor
Signal Transduction
description The neuregulin receptor tyrosine kinase Erb-b4, initially linked to early cardiac development, is shown here to play a critical role in adult cardiac function. In wild-type mice, Erb-b4 protein localized to Z lines and to intercalated disks, suggesting a role in subcellular and intercellular communications of cardiomyocytes. Conditional inactivation of erb-b4 in ventricular muscle cells led to a severe dilated cardiomyopathy, characterized by thinned ventricular walls with eccentric hypertrophy, reduced contractility, and delayed conduction. This cardiac dysfunction may account for premature death in adult erb-b4-knockout mice. This study establishes a critical role for Erb-b4 in the maintenance of normal postnatal cardiac structure and function. Copyright © 2005 the American Physiological Society.
title Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle
title_short Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle
title_full Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle
title_fullStr Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle
title_full_unstemmed Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle
title_sort dilated cardiomyopathy in erb-b4-deficient ventricular muscle
publishDate 2005
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03636135_v289_n358-3_pH1153_GarciaRivello
http://hdl.handle.net/20.500.12110/paper_03636135_v289_n358-3_pH1153_GarciaRivello
_version_ 1768543802602029056