Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-5-18
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/PRKCD protein, human, http://linkedlifedata.com/resource/pubmed/chemical/PRKCE protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine, http://linkedlifedata.com/resource/pubmed/chemical/Prkcd protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Prkce protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C-delta, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C-epsilon
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
286
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2195-203
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14975926-Adenoviridae, pubmed-meshheading:14975926-Animals, pubmed-meshheading:14975926-Cardiotonic Agents, pubmed-meshheading:14975926-Cell Division, pubmed-meshheading:14975926-Cells, Cultured, pubmed-meshheading:14975926-Gene Transfer Techniques, pubmed-meshheading:14975926-Humans, pubmed-meshheading:14975926-MAP Kinase Signaling System, pubmed-meshheading:14975926-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:14975926-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:14975926-Mitogen-Activated Protein Kinases, pubmed-meshheading:14975926-Myocytes, Cardiac, pubmed-meshheading:14975926-Phenylephrine, pubmed-meshheading:14975926-Protein Kinase C, pubmed-meshheading:14975926-Protein Kinase C-delta, pubmed-meshheading:14975926-Protein Kinase C-epsilon, pubmed-meshheading:14975926-Rats
pubmed:year
2004
pubmed:articleTitle
PKC-epsilon regulation of extracellular signal-regulated kinase: a potential role in phenylephrine-induced cardiocyte growth.
pubmed:affiliation
Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, 303 Thurmond Bldg., 114 Doughty Street, Charleston, SC 29403, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't