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1Department of Physiology, Faculty of Medicine; and 2Department of Human Nutritional Sciences, Faculty of Human Ecology, Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada
Submitted 24 November 2003 ; accepted in final form 8 March 2004
Volume overload due to arteriovenous (AV) shunt results in cardiac hypertrophy followed by the progression to heart failure. The phosphoinositide phospholipase C (PLC) converts phosphatidylinositol 4,5-bisphosphate (PIP2) to 1,2-diacylglycerol (DAG) and inositol (1,4,5)-trisphosphate (IP3), which are known to influence cardiac function. Therefore, we examined the time course of changes in DAG and IP3 as well as PLC isozyme gene expression, protein content, and activities in cardiac hypertrophy and heart failure induced by AV shunt in Sprague-Dawley rats by the needle technique. An increase in the left ventricle (LV)-to-body weight ratio demonstrated that LV hypertrophy was established at 4 wk after the induction of the shunt. PLC-
1 activity was increased two- and sevenfold at 3 days and 1 and 2 wk after the induction of volume overload, respectively. These changes were associated with increases in the mRNA and sarcolemmal (SL) protein content; however, no changes in PLC-1 were detected at 4 wk. On the other hand, a significant increase in PLC-
1 activity as well as mRNA and SL protein was seen at 3 days and 4 wk. A progressive decrease in PLC-
1 activity with concomitant reductions in the gene expression and SL protein abundance was detected during 1 to 4 wk. Activity of 1- and 1-isozymes was significantly depressed during the 8- and 16-wk time points, whereas 1-isozyme was increased significantly during these time points. A progressive decrease in the SL PIP2 content was observed during cardiac hypertrophy and heart failure. Our findings indicate that PLC isozyme signaling processes are increased in hypertrophy and decreased in heart failure due to volume overload.
cardiac sarcolemma; signal transduction
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