Phospholipase C gene expression, protein content, and activities in cardiac hypertrophy and heart failure due to volume overload

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 ar...

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Bibliographic Details
Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 56; no. 2; pp. 719 - 727
Main Authors DENT, Melissa R, DHALLA, Naranjan S, TAPPIA, Paramjit S
Format Journal Article
LanguageEnglish
Published Bethesda, MD American Physiological Society 01.08.2004
Subjects
Biological and medical sciences
Cardiology
Fundamental and applied biological sciences. Psychology
Gene expression
Heart failure
Proteins
Rodents
Vertebrates: cardiovascular system
Heart failure
Sarcolemma
cardiac sarcolemma
Enzyme
Cardiovascular disease
Protein C
Esterases
Phosphoric diester hydrolases
Gene expression
Heart volume
Phospholipase C
Signal transduction
Vertebrata
Mammalia
Overload
Heart disease
Hydrolases
Circulatory system
Protein content
Hypertrophy
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Summary: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. [PUBLICATION ABSTRACT]
ISSN:0363-6135
1522-1539