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Reports from St. Thomas' Hospital advance knowledge in perfusion
2009 AUG 17 - (NewsRx.com) -- According to recent research published in the journal Cardiovascular Research, "Despite their ability to cause septic shock and myocardial dysfunction, components of Gram-negative bacterial cell walls, like lipopolysaccharide, have been shown in numerous studies to induce myocardial protection during ischaemia-reperfusion injury. Muramyl dipeptide (MDP) is another such component recognized by an intracellular receptor, nucleotide-binding oligomerization domain 2. Receptor activation leads to intracellular signals through receptor interacting protein-2 (RIP2) and tumour growth factor-beta-activated kinase-1 (TAK1)." "However, little is known about the RIP2/TAK1 pathway in the heart. The aim of this study was to determine whether the RIP2/TAK1 pathway has a cardioprotective role in a mouse model of myocardial infarction. We isolated and subjected wild-type (WT) and RIP2(-/-) mouse hearts to 30 min of global ischaemia and 120 min of reperfusion with or without perfusion of MDP (10 mu g/mL) before or after the ischaemic period and determined the infarct size. We examined activation of the TAK1/nuclear factor kappa B (NF kappa B) signalling pathway. The effect of TAK1 inhibition on MDP-induced cardioprotection was also evaluated. Exposure to MDP during reperfusion significantly reduced infarct size in WT hearts (from 51.7 +/- 5.6% in control to 38.1 +/- 6.7%, P< 0.05), but not in RIP2(-/-) hearts or in WT hearts with coincident pharmacological inhibition of TAK1. MDP treatment significantly increased the levels of p-TAK1 and p-JNK (Jun N-terminal kinase) and led to NF kappa B activation via phosphorylation and degradation of IkappaB in the WT, but not in the RIP2(-/-), myocardium," wrote P. Sicard and colleagues, St. Thomas' Hospital. The researchers concluded: "These results indicate that MDP at reperfusion induced cardioprotection through an RIP2/TAK1-dependent mechanism.." Sicard and colleagues published their study in Cardiovascular Research (Pharmacological postconditioning effect of muramyl dipeptide is mediated through RIP2 and TAK1. Cardiovascular Research, 2009;83(2):277-284). For additional information, contact S. Jacquet, Kings College London, British Heart Foundation Center Research Excellence, Division Cardiovascular, Rayne Institute, St. Thomas Hospital, Lambeth Palace Rd., London SE1 7EH, UK. The publisher's contact information for the journal Cardiovascular Research is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England. Keywords: United Kingdom, London, Blood Transfusion, Cardiology, Cardioprotection, Cardiovascular, Enzyme Research, Gram-Negative Bacterial, Heart Attack, Ischemia-Reperfusion Injury, Kinase, Medical Device, Myocardial Infarction, Peptide, Perfusion, Pharmaceuticals, Pharmacological, Proteins, Proteomics, Reperfusion, Septic Shock, Transfusion Medicine, St. Thomas' Hospital. This article was prepared by Cardiovascular Week editors from staff and other reports. Copyright 2009, Cardiovascular Week via NewsRx.com.
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