Mice lacking the C[beta] subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction

Abstract Background: PKA is a ubiquitous, multi-subunit cellular kinase that regulates a number of different physiological responses in response to cAMP, including metabolism, cell division, and cardiac function. Numerous studies have implicated altered PKA signaling in cardiac dysfunction. Recently...

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Bibliographic Details
Published in:BMC research notes 2010-01, Vol.3, p.307
Main Authors: Enns, Linda C, Bible, Kenneth L, Emond, Mary J, Ladiges, Warren C
Format: Article
Language:English
Subjects:
Blood pressure
Cardiomyocytes
Colleges & universities
Hypertension
Kinases
Phosphorylation
Protein synthesis
Proteins
Rodents
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Summary:Abstract Background: PKA is a ubiquitous, multi-subunit cellular kinase that regulates a number of different physiological responses in response to cAMP, including metabolism, cell division, and cardiac function. Numerous studies have implicated altered PKA signaling in cardiac dysfunction. Recently, it has been shown that mice lacking the catalytic β subunit of PKA (PKA Cβ) are protected from age-related problems such as weight gain and enlarged livers, and we hypothesized that these mice might also be resistant to cardiomyopathy. Findings: Angiotensin II (ang II) induced hypertension in both PKA Cβ null mice and their WT littermates. However, PKA Cβ null mice were resistant to a number of ang II-induced, cardiopathological effects observed in the WT mice, including hypertrophy, decreased diastolic performance, and enlarged left atria. Conclusion: The Cβ subunit of PKA plays an important role in angiotensin-induced cardiac dysfunction. The Cβ null mouse highlights the potential of the PKA Cβ subunit as a pharmaceutical target for hypertrophic cardiac disease.
ISSN:1756-0500
DOI:10.1186/1756-0500-3-307