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

Author:

Sentex Emmanuelle1,Wang Xi1,Liu Xueliang1,Lukas Anton1,Dhalla Naranjan S.1

Affiliation:

1. Institute of Cardiovascular Sciences St. Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine University of Manitoba, 351 Tache Avenue, Winnipeg, MB R2H 2A6, Canada.

Abstract

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-α and PKC-ζ contents at 2 week and increases in PKC-α, PKC-β1, PKC-β2, and PKC-ζ 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 Gαq was increased in the LV at 2 weeks but then decreased at 16 weeks, whereas Gαq 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.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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