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We have found that the acute inflammation accompanying myocardial infarction begins shortly after reperfusion and enlarges the area of irreversible injury. Limiting inflammation by various means, such as with antibodies or drugs, can reduce infarct size and improve left ventricular function. Inflammation begins with conversion of endothelial cells in the ischemic myocardium to a pro-inflammatory phenotype, with increased expression of leukocyte adhesion proteins, such as intercellular adhesion molecule-1 (ICAM-1), and microvascular trapping of neutrophils with accumulation in the myocardium.
ICAM-1 gene upregulation in the post-ischemic myocardium is mediated by tumor necrosis factor [alpha] (TNF[alpha]) through the NFkB pathway, but also by activation (phosphorylation) of the transcription factor Stat3, bound to the transcriptional activator Sp1. Stat3 is phosphorylated in turn by interaction with Rac1, an essential subunit of the endothelial NADPH oxidase, through a novel multiprotein complex involving Stat3, Rac1, and protein kinase C (PKC).