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Carbonic anhydrase II promotes cardiomyocyte hypertrophy Open Access


Other title
carbonic anhydrase
transport metabolon
heart failure
bicarbonate transport
Type of item
Degree grantor
University of Alberta
Author or creator
Brown, Brittany Fielding
Supervisor and department
Casey, Joseph (Biochemistry)
Examining committee member and department
Leslie, Elaine (Physiology)
Fliegel, Larry (Biochemistry)
Department of Physiology

Date accepted
Graduation date
Master of Science
Degree level
Cardiac hypertrophy is maladaptive remodeling of the myocardium that often progresses to heart failure. The hypertrophic transport metabolon consists of membrane transporters implicated in hypertrophy, and substrates for these transporters are provided by the catalytic action of carbonic anhydrase II (CAII). CAII inhibition prevents and reverts cardiomyocyte hypertrophy in vitro, suggesting that CAII is an important protein in the development of hypertrophy. To explore this further, neonatal rat ventricular myocytes (NRVMs) were transduced with adenoviral constructs to overexpress wild type or catalytically inactive CAII. Upon treatment with phenylephrine, NRVMs overexpressing catalytically inactive CAII exhibited reduced cardiac remodeling associated with hypertrophy. Cardiomyocytes isolated from a line of mice with a null mutation in the CAII gene were also protected from hypertrophic stimulation. The findings of these studies support the importance of CAII in the promotion of cardiac hypertrophy, and may potentially lead to new therapeutic strategies for heart failure.
License granted by Brittany Brown ( on 2011-12-07T18:24:17Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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