Why the study?
Does conditional inactivation of erb-b4 in ventricular muscle cells lead to cardiac dysfunction in adult mice?
Does conditional inactivation of erb-b4 in ventricular muscle cells lead to cardiac dysfunction in adult mice?
The study establishes a critical role for the neuregulin receptor tyrosine kinase Erb-b4 in maintaining normal postnatal cardiac structure and function.
ErbB4 maintains postnatal cardiac structure in mice; hypothesis-generating for neuregulin pathway targeting in human cardiomyopathy.
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.
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Rivello et al. (2005) studied this question.
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