Does loss of AKAP121 precede induction of cardiac hypertrophy?
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Date
2012-03-12
Authors
Cheung, Anene
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Abstract
The A‐kinase anchor proteins (AKAPs) are diverse regulators of cell function, acting as scaffolds
to co‐localize the protein kinase A regulatory sub‐unit with target proteins, such as other
kinases and phosphatases. We have previously demonstrated that over‐expression of AKAP121
in cardiomyocytes attenuates hypertrophy induced by isoproterenol. Furthermore, knockdown
of AKAP121 expression induced spontaneous cardiomyocyte hypertrophy, suggesting that
AKAP121 behaves as a potent anti‐hypertrophic regulator. In this study, mice underwent
transverse aortic constriction (TAC), resulting in increased cardiac afterload and progressive
hypertrophy. Quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blotting
was used to examine expression of AKAP121 in banded and sham control animals. The degree
of hypertrophy was assessed by heart weight to body weight or tibia length ratios. We
hypothesized that AKAP121 expression will decrease soon after banding, prior to frank
hypertrophy. Our current results demonstrate a correlation between loss of AKAP121
expression and induction of the hypertrophic gene program in response to pressure overload
induced by thoracic aortic banding, thus indicating a potential role for AKAP121 as a regulator of
the hypertrophic response in vivo. Our data also suggests that a sex‐specific mechanism may be
involved in regulation of hypertrophic gene expression.
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medicine