Increased expression of protein kinase C isoforms in heart failure due to myocardial infarction

American Journal of Physiology - Heart and Circulatory Physiology - Tập 284 Số 6 - Trang H2277-H2287 - 2003
Jingwei Wang1, Xueliang Liu1, Emmanuelle Sentex1, Nobuakira Takeda2, Naranjan S. Dhalla1
1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6; and
2Aoto Hospital, Jikei University, Tokyo 125-8506, Japan

Tóm tắt

The activities of cardiac protein kinase C (PKC) were examined in hemodynamically assessed rats subsequent to myocardial infarction (MI). Both Ca2+-dependent and Ca2+-independent PKC activities increased significantly in left ventricular (LV) and right ventricular (RV) homogenates at 1, 2, 4, and 8 wk after MI was induced. PKC activities were also increased in both LV and RV cytosolic and particulate fractions from 8-wk infarcted rats. The relative protein contents of PKC-α, -β, -ε, and -ζ isozymes were significantly increased in LV homogenate, cytosolic (except PKC-α), and particulate fractions from the failing rats. On the other hand, the protein contents of PKC-α, -β, and -ε isozymes, unlike the PKC-ζ isozyme, were increased in RV homogenate and cytosolic fractions, whereas the RV particulate fraction showed an increase in the PKC-α isozyme only. These changes in the LV and RV PKC activities and protein contents in the 8-wk infarcted animals were partially corrected by treatment with the angiotensin-converting enzyme inhibitor imidapril. No changes in protein kinase A activity and its protein content were seen in the 8-wk infarcted hearts. The results suggest that the increased PKC activity in cardiac dysfunction due to MI may be associated with an increase in the expression of PKC-α, -β, and -ε isozymes, and the improvement of heart function in the infarcted animals by imidapril may be due to partial prevention of changes in PKC activity and isozyme contents.

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American Journal of Physiology - Heart and Circulatory Physiology

Tập 284 Số 6

H2277-H2287

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