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Expression of protein kinase C isoforms in cardiac hypertrophy and heart failure due to volume overload.

Authors: Sentex, E  Wang, X  Liu, X  Lukas, A  Dhalla, NS 
Citation: Sentex E, etal., Can J Physiol Pharmacol. 2006 Feb;84(2):227-38.
Pubmed: (View Article at PubMed) PMID:16900949
DOI: Full-text: DOI:10.1139/y05-120

The present study determined whether changes in the activity and isoforms of protein kinase C (PKC) are associated with cardiac hypertrophy and heart failure owing to volume overload induced by aortocaval shunt (AVS) in rats. A significant increase in Ca2+-dependent and Ca2+-independent PKC activities in the homogenate and particulate fractions, unlike the cystolic fraction, of the hypertrophied left ventricle (LV) were evident at 2 and 4 weeks after inducing the AVS. This increase coincided with increases in PKC-alpha and PKC-zeta contents at 2 week and increases in PKC-alpha, PKC-beta1, PKC-beta2, and PKC-zeta contents at 4 weeks in the hypertrophied LV. By 8 and 16 weeks of AVS, PKC activity and content were unchanged in the failing LV. On the other hand, no increase in the PKC activity or isoform content in the hypertrophied right ventricle (RV) was observed during the 16 weeks of AVS. The content of G alpha q was increased in the LV at 2 weeks but then decreased at 16 weeks, whereas G alpha q content was increased in RV at 2 and 4 weeks. Our data suggest that an increase in PKC isoform content neither plays an important role during the development of cardiac hypertrophy nor participates in the phase leading to heart failure owing to volume overload.


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CRRD Object Information
CRRD ID: 1581275
Created: 2006-09-25
Species: All species
Last Modified: 2006-09-25
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.