Activation of poly(ADP-ribose) polymerase in circulating leukocytes during myocardial infarction.

Kanneganti G.K. Murthy, Chun Yang Xiao, Jon G. Mabley, Min Chen, Csaba Szabó

    Research output: Contribution to journalArticle

    26 Scopus citations

    Abstract

    Myocardial ischemia-reperfusion can lead to increased oxidative stress both locally and in circulating leukocytes. Oxidant-mediated DNA single strand breaks are known to activate the nuclear enzyme poly(ADP-ribose) polymerase (PARP) in various forms of shock, inflammation, and ischemia-reperfusion injury. The aim of the current study was to investigate whether a local insult such as myocardial ischemia-reperfusion is sufficient to lead to activation of PARP in circulating leukocytes. In anesthetized rats myocardial ischemia-reperfusion was induced by transient ligation of the left anterior descending coronary artery. There was a marked increase in poly(ADP-ribosyl)ation of proteins in homogenates of leukocytes isolated from rats at the end of the reperfusion period. Poly(ADP-ribosyl)ation was inhibited by administration of the pharmacologic PARP inhibitor INO-1001 (30 mg/kg) to the rats. We conclude that local insults, such as myocardial reperfusion injury, are sufficient to activate PARP in circulating leukocytes. PARP activation in circulating cells may mediate certain systemic effects of local ischemia-reperfusion injury such as inflammatory mediator production and remote organ injury.

    Original languageEnglish (US)
    Pages (from-to)230-234
    Number of pages5
    JournalShock (Augusta, Ga.)
    Volume21
    Issue number3
    DOIs
    StatePublished - Mar 2004

    ASJC Scopus subject areas

    • Emergency Medicine
    • Critical Care and Intensive Care Medicine

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