Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response

Figures

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  Figure 1. Norepinephrine-induced signal transduction resulting in cardiomyocyte hypertrophy. α1-AR, α1-adrenoceptors; Gαq, Gq protein alpha subunit; PLC, phospholipase C. There are several proteins that are phosphorylated such as ERK1/2, PKC, Ca2+/Calmodulin-dependent kinase, and JNK [32], which in turn phosphorylate and activate transcription factors such as c-Fos and c-Jun leading to the gene expression of PLC as well as the expression of fetal genes that are characteristic of cardiac hypertrophy [9,33].

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  Figure 2. Role of phospholipase C in the perpetuation of cardiomyocyte growth response to norepinephrine. DAG = sn-1,2-diacylglycerol; IP3, inositol-1,4,5-trisphosphate. The response to increased levels of norepinephrine (input) is a cyclical process that produces an increase in the expression of PLC isozyme genes and subsequent higher generation of DAG and IP3 and stimulation of the signal for cardiac hypertrophy (output). The activation and amplification of PLC isozymes ensure continuation of this cycle of events for continuation of abnormal hypertrophic growth due sustained exposure to high levels of norepinephrine.