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Temporal changes in myocardial salvage kinases during reperfusion following ischemia: Studies involving the cardioprotective adipocytokine apelin

Simpkin, JC; Dixon, RA; Cooper, MB; Yellon, DM; (2007) Temporal changes in myocardial salvage kinases during reperfusion following ischemia: Studies involving the cardioprotective adipocytokine apelin. CARDIOVASC DRUG THER , 21 (6) 409 - 414. 10.1007/s10557-007-6054-y.

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Abstract

Introduction Activation of the Reperfusion Injury Salvage Kinase (RISK) pathway, which incorporates phosphatidylinositol-3-OH kinase (PI3K)-Akt/protein kinase B (PKB) and p44/42 mitogen-activated protein kinase (MAPK), underlies protection against ischemia-reperfusion (I/R) injury. The temporal nature of the activation of these RISK pathway components during reperfusion is, however, uncertain. We examined Akt and p44/42 phosphorylation in hearts subjected to ischemia and varying periods of reperfusion in the absence or presence of the putative cardioprotectant, apelin-13. Akt activity was also measured.Materials and methods Langendorff perfused C57Bl/6J mouse hearts were subjected to 35 min global ischemia followed by 0, 2.5, 5 or 10 min reperfusion with or without 1 mu M apelin-13. Basal and apelin-induced phosphorylation of Akt (at both the threonine 308 and serine 473 phosphorylation sites) and p44/42 during the reperfusion phase was determined by Western blotting and Akt activity measured using an Enzyme-Linked ImmunoSorbent Assay (ELISA).Results Basal phosphorylation of both Akt and p44/42 increased progressively with time of reperfusion. Apelin enhanced Akt and p44/42 phosphorylation at all reperfusion time points. Akt activity did not change under basal conditions but was increased by apelin at 5 min (NS) and 10 min (p < 0.05) reperfusion.Discussion We conclude that under basal conditions Akt and p44/42 phosphorylation increases with time of reperfusion but that this is not accompanied by increased kinase (Akt) activity. On application of a cardioprotectant, however, kinase phosphorylation and activity are enhanced suggesting that it is the combination of these two mechanisms that may underly the tissue preserving actions of such agents.

Type: Article
Title: Temporal changes in myocardial salvage kinases during reperfusion following ischemia: Studies involving the cardioprotective adipocytokine apelin
DOI: 10.1007/s10557-007-6054-y
Keywords: myocardium, ischemia-reperfusion injury, salvage kinases, temporal changes, HEART, SURVIVAL, INJURY, CARDIOMYOCYTES, ATORVASTATIN, ACTIVATION, PROTECTS
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 > Hatter Cardiovascular Institute
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
URI: http://discovery.ucl.ac.uk/id/eprint/179447
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