AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 286: H2195-H2203, 2004. First published February 19, 2004; doi:10.1152/ajpheart.00475.2003
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PKC-{epsilon} regulation of extracellular signal-regulated kinase: a potential role in phenylephrine-induced cardiocyte growth

Vijay U. Rao, Hirokazu Shiraishi, and Paul J. McDermott

Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, and the Ralph H. JohnsonVeterans Affairs Medical Center, Charleston, South Carolina 29425-2221

Submitted 22 May 2003 ; accepted in final form 9 February 2004

Hypertrophic growth of cardiac muscle is dependent on activation of the PKC-{epsilon} isoform. To define the effectors of PKC-{epsilon} involved in growth regulation, recombinant adenoviruses were used to overexpress either wild-type PKC-{epsilon} (PKC-{epsilon}/WT) or dominant negative PKC-{epsilon} (PKC-{epsilon}/DN) in neonatal rat cardiocytes. PKC-{epsilon}/DN inhibited acute activation of PKC-{epsilon} produced in response to phorbol ester and reduced ERK1/2 activity as measured by the phosphorylation of p42 and p44 isoforms. The inhibitory effects were specific to PKC-{epsilon} because PKC-{epsilon}/DN did not prevent translocation of either PKC-{alpha} or PKC-{delta}. Overexpression of PKC-{epsilon}/DN blunted the acute increase in ERK1/2 phorphorylation induced by the {alpha}1-adrenergic agonist phenylephrine (PE ). Inhibition of PKC-{delta} with rottlerin potentiated the effects of PE on ERK1/2 phosphorylation. PKC-{epsilon}/DN adenovirus also blocked cardiocyte growth as measured after 48 h of PE treatment, although the multiplicity of infection was lower than that required to block acute ERK1/2 activation. PE activated p38 mitogen-activated protein kinase as measured by its phosphorylation, but the response was not blocked by PKC inhibitors or by overexpression of PKC-{epsilon}/DN. Taken together, these studies show that the hypertrophic agonist PE regulates ERK1/2 activity in cardiocytes by a pathway dependent on PKC-{epsilon} and that PE-induced growth is mediated by PKC-{epsilon}.

heart; hypertrophy; cell signaling; mitogen-activated protein kinase


Address for reprint requests and other correspondence: P. J. McDermott, 303 Thurmond Bldg., 114 Doughty St., Charleston, SC 29403 (E-mail: mcdermp{at}musc.edu).




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