UCL logo

UCL Discovery

UCL home » Library Services » Electronic resources » UCL Discovery

Cardioprotection mediated by urocortin is dependent upon PKCF epsilon activation

Lawrence, KM; Kabir, AMN; Bellahcene, M; Davidson, S; Mesquita, RS; Cao, XB; McCormick, J; ... Latchman, DS; + view all (2005) Cardioprotection mediated by urocortin is dependent upon PKCF epsilon activation. FASEB J , 19 (3) 831 - +. 10.1096/fj.04-2506fje.

Full text not available from this repository.

Abstract

Urocortin (Ucn) is an endogenous cardioprotective agent that protects against the damaging effects of ischemia and reperfusion injury in vitro and in vivo. We have found that the mechanism of action of Ucn involves both acute activation of specific target molecules, and using Affymetrix (Santa Clara, CA) gene chip technology, altered gene expression of different end effector molecules. Here, from our gene chip data, we show that after a 24 h exposure to Ucn, there was a specific increase in mRNA and protein levels of the protein kinase C epsilon (PKC epsilon) isozyme in primary rat cardiomyocytes compared with untreated cells and in the Langendorff perfused ex vivo heart. Furthermore, a short 10 min exposure of these cells to Ucn caused a specific translocation/activation of PKC epsilon, in vitro and in the Langendorff perfused ex vivo heart. The importance of the PKC epsilon, isozyme in cardioprotection and its relationship to cardioprotection produced by Ucn was assessed using PKC epsilon-specific inhibitor peptides. The inhibitor peptide, when introduced into cardiomyocytes, caused an increase in apoptotic cell death compared with control peptide after ischemia and reperfusion. When the inhibitor peptide was present with Ucn, the cardioprotective effect of Ucn was lost. This loss of cardioprotection by Ucn was also seen in whole hearts from PKC epsilon, knockout mice. These findings indicate that the cardioprotective effect of Ucn is dependent upon PKC epsilon.

Type: Article
Title: Cardioprotection mediated by urocortin is dependent upon PKCF epsilon activation
DOI: 10.1096/fj.04-2506fje
Keywords: ischemia, protein kinase C epsilon, apoptosis, mitochondria, PROTEIN-KINASE-C, CARDIAC MYOCYTES, REPERFUSION INJURY, GENE-EXPRESSION, ISCHEMIC-INJURY, MOUSE HEARTS, DELTA-PKC, LOCALIZATION, PEPTIDES, PROTECTION
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Institute of Cardiovascular Science
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Institute of Cardiovascular Science > Pre-clinical and Fundamental Science
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > UCL GOS Institute of Child Health
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > UCL GOS Institute of Child Health > ICH - Directors Office
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > UCL GOS Institute of Child Health > ICH Genetics and Genomic Medicine Prog
URI: http://discovery.ucl.ac.uk/id/eprint/167508
Downloads since deposit
0Downloads
Download activity - last month
Download activity - last 12 months
Downloads by country - last 12 months

Archive Staff Only

View Item View Item