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1 Institute of Cardiovascular Sciences, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
2 Institute of Cardiovascular Sciences, Department of Human Nutritional Sciences, Faculty of Human Ecology, University of Manitoba, Winnipeg, Manitoba, Canada
* To whom correspondence should be addressed. E-mail: ptappia{at}sbrc.ca.
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 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 weeks after the induction of the shunt. PLC 
1 activity was increased 2- and 7-fold at 3 day, 1 and 2 weeks 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 weeks. 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 weeks. A progressive decrease in PLC 
1 activity with concomitant reductions in the gene expression and SL protein abundance was detected during 1 to 4 weeks. Activity of 1, and 1 isozymes was significantly depressed during the 8 and 16-week time points, whereas 1 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.
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