Inositol polyphosphate 1-phosphatase is a novel antihypertrophic factor.
Abstract
Activation of G(q)-coupled alpha(1)-adrenergic receptors leads to hypertrophic growth of neonatal rat ventricular cardiomyocytes that is associated with increased expression of hypertrophy-related genes, including atrial natriuretic peptide (ANP) and myosin light chain-2 (MLC), as well as increased ribosome synthesis. The role of inositol phosphates in signaling pathways involved in these changes in gene expression was examined by overexpressing inositol phosphate-metabolizing enzymes and determining effects on ANP, MLC, and 45 S ribosomal gene expression following co-transfection of appropriate reporter gene constructs. Overexpression of enzymes that metabolize inositol 1,4,5-trisphosphate did not reduce ANP or MLC responses, but overexpression of the enzyme primarily responsible for metabolism of inositol 4,5-bisphosphate (Ins(1,4)P(2)), inositol polyphosphate 1-phosphatase (INPP), reduced ANP and MLC responses associated with alpha(1)-adrenergic receptor-mediated hypertrophy. Similarly overexpressed INPP reduced ANP and MLC responses associated with contraction-induced hypertrophy. In addition, overexpression of INPP reduced the increase in ribosomal DNA transcription associated with both hypertrophic models. Hypertrophied c...Continue Reading
References
Ins(3,4,5,6)P4 specifically inhibits a receptor-mediated Ca2+-dependent Cl- current in CFPAC-1 cells
CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo
Citations
MicroRNA-26 was decreased in rat cardiac hypertrophy model and may be a promising therapeutic target
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