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

Temporal changes in myocardial salvage kinases during reperfusion following ischemia: studies involving the cardioprotective adipocytokine apelin. Research Abstract Details 

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Temporal changes in myocardial salvage kinases during reperfusion following ischemia: studies involving the cardioprotective adipocytokine apelin. Abstract Text:

Christopher C T Smith,Michaela M Mocanu,Jonathan Bowen,Abigail M Wynne,James C Simpkin,Richard A Dixon,Michael B Cooper,Derek M Yellon,Christopher C T Smith,Michaela M Mocanu,Jonathan Bowen,Abigail M Wynne,James C Simpkin,Richard A Dixon,Michael B Cooper,Derek M Yellon,Christopher C T Smith,Michaela M Mocanu,Jonathan Bowen,Abigail M Wynne,James C Simpkin,Richard A Dixon,Michael B Cooper,Derek M Yellon,

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 microM 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.

Temporal changes in myocardial salvage kinases during reperfusion following ischemia: studies involving the cardioprotective adipocytokine apelin. Publishing Authors By Initials

CC Smith,MM Mocanu,J Bowen,AM Wynne,JC Simpkin,RA Dixon,MB Cooper,DM Yellon,CC Smith,MM Mocanu,J Bowen,AM Wynne,JC Simpkin,RA Dixon,MB Cooper,DM Yellon,CC Smith,MM Mocanu,J Bowen,AM Wynne,JC Simpkin,RA Dixon,MB Cooper,DM Yellon,

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Temporal changes in myocardial salvage kinases during reperfusion following ischemia: studies involving the cardioprotective adipocytokine apelin. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Cardiovascular drugs and therapy / sponsored by th

VOLUME: 21

Page Numbers: 409-14

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ISSN: 0920-3206

DAY: 6

MONTH: Dec

YEAR: 2007

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

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LANGUAGE: eng

NlmUniqueID: 8712220

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AFFILIATION: The Hatter Cardiovascular Institute, University College London Hospital and Medical School, 67 Chenies Mews, London, WC1E 6HX, UK.

Country: United States

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MEDLINETA: Cardiovasc Drugs Ther

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