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Protein kinase C--induced hypertrophy of neonatal rat ventricular myocytes

Cardiovascular Institute, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153

Submitted 23 February 2004 ; accepted in final form 19 July 2004

Protein kinase C (PKC) isoenzymes play a critical role in cardiomyocyte hypertrophy. At least three different phorbol ester-sensitive PKC isoenzymes are expressed in neonatal rat ventricular myocytes (NRVMs): PKC-, -, and -. Using replication-defective adenoviruses (AdVs) that express wild-type (WT) and dominant-negative (DN) PKC- together with phorbol myristate acetate (PMA), which is a hypertrophic agonist and activator of all three PKC isoenzymes, we studied the role of PKC- in signaling-specific aspects of the hypertrophic phenotype. PMA induced nuclear translocation of endogenous and AdV-WT PKC- in NRVMs. WT PKC- overexpression increased protein synthesis and the protein-to-DNA (P/D) ratio but did not affect cell surface area (CSA) or cell shape compared with uninfected or control AdV -galactosidase (AdV gal)-infected cells. PMA-treated uninfected cells displayed increased protein synthesis, P/D ratio, and CSA and elongated morphology. PMA did not further enhance protein synthesis or P/D ratio in AdV-WT PKC--infected cells. To assess the requirement of PKC- for these PMA-induced changes, AdV-DN PKC- or AdV gal-infected NRVMs were stimulated with PMA. Without PMA, AdV-DN PKC- had no effects on protein synthesis, P/D ratio, CSA, or shape vs. AdV gal-infected NRVMs. PMA increased protein synthesis, P/D ratio, and CSA in AdV gal-infected cells, but these parameters were significantly reduced in PMA-stimulated AdV-DN PKC--infected NRVMs. Overexpression of DN PKC- enhanced PMA-induced cell elongation. Neither WT PKC- nor DN PKC- affected atrial natriuretic factor gene expression. Insulin-like growth factor-1 also induced nuclear translocation of endogenous PKC-. PMA but not WT PKC- overexpression induced ERK1/2 activation. However, AdV-DN PKC- partially blocked PMA-induced ERK activation. Thus PKC- is necessary for certain aspects of PMA-induced NRVM hypertrophy.

signal transduction; heart; adenovirus; translocation

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