© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Differential regulation of cardiac protein kinase C isozyme expression after aortic banding in rat
aDepartment of Cardiology, Medical Clinic II, University of Technology Dresden, Fetscherstr. 76, 01307 Dresden, Germany
bDepartment of Cardiology, Medical Center, University of Mannheim, Mannheim, Germany
cDepartment of Cardiology, Angiology and Pulmology, Medical Center, University of Heidelberg, Heidelberg, Germany
ruth.strasser{at}mailbox.tu-dresden.de
* Corresponding author. Tel.: +49-351-450-1700; fax: +49-351-450-1702
Objective: Protein kinase C (PKC) plays a key role in myocardial hypertrophy. To evaluate whether its isoforms are expressed differentially during gradual development of pressure-overload-induced cardiac hypertrophy, banding of the ascending aorta was used as an experimental model of left ventricular hypertrophy. Methods: One, 7 and 30 days after sham operation or aortic banding in male Wistar rats, the PKC activity and the expression of the cardiac PKC isozymes (PKC-
, -
, -
and -
), both at the protein and the mRNA level, were determined in the left and right ventricle. Results: Left ventricular hypertrophy developed rapidly as early as 1 day after aortic banding followed by further progression at day 7 and day 30. This was paralleled by an increased total PKC enzyme activity in the cytosol fraction and a selectively enhanced protein expression of PKC- (day 7, 267±18%; day 30, 289±12%) and PKC- (day 7, 212±20%; day 30, 193±14%). The protein amount of PKC- was not changed in either group. This differential protein expression was associated with a significant increase of the absolute mRNA levels for PKC- and PKC- up to 202±20% (day 30) and 177±17% (day 30), whereas significant alterations in the PKC- mRNA levels were not detected. A selective upregulation of PKC- and PKC-, both on the protein and on the mRNA level, was also noted in the right ventricle during the development of right ventricular hypertrophy, suggesting an adaptive response following elevated left ventricular enddiastolic pressure after long-term aortic banding for 30 days. Conclusions: This study characterizes in the right and left ventricle a differential regulation of the dominant PKC isozymes in pressure-overload cardiac hypertrophy both at the protein and the mRNA level.
KEYWORDS Gene expression; Hypertrophy; Protein kinases; Signal transduction; Ventricular function
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