Expression of protein kinase C beta in the heart causes hypertrophy in adult mice and sudden death in neonates

Protein kinase C (PKC) activation in the heart has been linked to a hypertrophic phenotype and to processes that influence contractile function. To establish whether PKC activation is sufficient to induce an abnormal phenotype, PKCbeta was conditionally expressed in cardiomyocytes of transgenic mice...

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Bibliographic Details
Published in:The Journal of clinical investigation 1997-11, Vol.100 (9), p.2189-2195
Main Authors: Bowman, J C, Steinberg, S F, Jiang, T, Geenen, D L, Fishman, G I, Buttrick, P M
Format: Article
Language:English
Subjects:
Age Factors
Animals
Animals, Newborn
Body Weight
Calcium - physiology
Cardiomegaly - enzymology
Death, Sudden
Female
Isoenzymes - metabolism
Isoproterenol - pharmacology
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Myocardium - enzymology
Protein Kinase C - metabolism
Protein Kinase C beta
Sarcomeres - physiology
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Summary:Protein kinase C (PKC) activation in the heart has been linked to a hypertrophic phenotype and to processes that influence contractile function. To establish whether PKC activation is sufficient to induce an abnormal phenotype, PKCbeta was conditionally expressed in cardiomyocytes of transgenic mice. Transgene expression in adults caused mild and progressive ventricular hypertrophy associated with impaired diastolic relaxation, whereas expression in newborns caused sudden death associated with marked abnormalities in the regulation of intracellular calcium. Thus, the PKC signaling pathway in cardiocytes has different effects depending on the timing of expression and, in the adult, is sufficient to induce pathologic hypertrophy.
ISSN:0021-9738
DOI:10.1172/jci119755