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Articles in PresS, published online ahead of print October 23, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00336.2002
Submitted on July 19, 2002
Accepted on October 19, 2002
1 Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA
2 Children's Hospital Medical Center, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: robbieg{at}scripps.edu.
Adenoviral gene transfer of constitutively active calcineurin into cells resulted in decreased mitochondrial membrane potential and increased superoxide production. Transgenic mice with cardiac-specific expression of a constitutively active calcineurin cDNA (CalTG mice) exhibit cardiac hypertrophy that progresses to failure. Intact, well-coupled subsarcolemmal mitochondria prepared from 1 to 2 mouse hearts at a time yielded sufficient material for studies of oxygen consumption. CalTG mice exhibited decreased respiration. Mitochondrial respiration was unaffected in tropomodulin overexpressing transgenic mice, another model of cardiomyopathy. Western blotting of mitochondria from CalTG mice revealed a decrease in the abundance of subunit 3 of complex I, and subunits I and IV of cytochrome oxidase, compared to littermate controls. Impaired mitochondrial electron transport was associated with high levels of superoxide production in the CalTG mice. We conclude that calcineurin signaling affects mitochondrial energetics and superoxide production. Excessive superoxide production may contribute to the development of cardiac failure.
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