We are analyzing https://link.springer.com/article/10.1007/s00395-010-0083-6.

Title:
Direct relationship between levels of TNF-α expression and endothelial dysfunction in reperfusion injury | Basic Research in Cardiology
Description:
We previously found that myocardial ischemia/reperfusion (I/R) initiates expression of tumor necrosis factor-α (TNF) leading to coronary endothelial dysfunction. However, it is not clear whether there is a direct relationship between levels of TNF expression and endothelial dysfunction in reperfusion injury. We studied levels of TNF expression by using different transgenic animals expressing varying amounts of TNF in I/R. We crossed TNF overexpression (TNF++/++) with TNF knockout (TNF−/−) mice; thus we have a heterozygote population of mice with the expression of TNF “in between” the TNF−/− and TNF++/++ mice. Mouse hearts were subjected to 30 min of global ischemia followed by 90 min of reperfusion and their vasoactivity before and after I/R was examined in wild type (WT), TNF−/−, TNF++/++ and TNF heterozygote (TNF−/++, cross between TNF−/− and TNF++/++) mice. In heterozygote TNF−/++ mice with intermediate cardiac-specific expression of TNF, acetylcholine-induced or flow-induced endothelial-dependent vasodilation following I/R was between TNF++/++ and TNF−/− following I/R. Neutralizing antibodies to TNF administered immediately before the onset of reperfusion-preserved endothelial-dependent dilation following I/R in WT, TNF−/++ and TNF++/++ mice. In WT, TNF−/++ and TNF++/++ mice, I/R-induced endothelial dysfunction was progressively lessened by administration of free-radical scavenger TEMPOL immediately before initiating reperfusion. During I/R, production of superoxide (O2 ·−) was greatest in TNF++/++ mice as compared to WT, TNF−/++ and TNF−/− mice. Following I/R, arginase mRNA expression was elevated in the WT, substantially elevated in the TNF−/++ and TNF++/++ mice and not affected in the TNF−/− mice. These results suggest that the level of TNF expression determines arginase expression in endothelial cells during myocardial I/R, which is one of the mechanisms by which TNF compromises coronary endothelial function in reperfusion injury.
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google, scholar, article, pubmed, cas, tnf, endothelial, dysfunction, zhang, mice, res, coronary, injury, basic, expression, reperfusion, cardiol, myocardial, necrosis, heart, tumor, lefer, role, physiol, circ, tnfalpha, research, ischemiareperfusion, ischemia, factoralpha, potter, nitric, privacy, cookies, content, levels, gao, arginase, access, effect, heusch, med, publish, search, vasodilation, cells, failure, factor, arterioles, schulz,

Topics {✒️}

month download article/chapter reperfusion-preserved endothelial-dependent dilation tumor necrosis factor-alpha tumor necrosis factor-α cachectin/tumor necrosis factor flow-induced endothelial-dependent vasodilation intermediate cardiac-specific expression ischaemia–reperfusion microvascular damage ischemia/reperfusion-induced endothelial dysfunction tumor necrosis factor ikk-beta pathway contributes maturation-induces endothelial dysfunction /r-induced endothelial dysfunction tnf-alpha potentiates oxidant nf-kappab pritchard ka jr article basic research vascular inflammation gp130-stat axis tnf-alpha-induced impairment endothelium-mediated vasodilation reperfusion-induced endothelial activation full article pdf microcirculation vasodilation access ischemic feline myocardium nitric oxide privacy choices/manage cookies atorvastatin research award endothelium-dependent vasodilation tnf-alpha contributes heart failure anti-edrf effect endothelium-dependent vasorelaxation recombinant human cachectin related subjects feed-forward signaling tissue injury induced atherosclerotic plaque composition ischemia/reperfusion injury ischemia-induced mechanisms coronary endothelial dysfunction tnf administered immediately myocardial ischemia/reperfusion ameliorating reperfusion injury article zhang european economic area left ventricular remodelling van de sand postischemic/reperfused myocardium dorn gw 2nd

Questions {❓}

Garcia SC, Pomblum V, Gams E, Langenbach MR, Schipke JD (2007) Independency of myocardial stunning of endothelial stunning?
Schulz R, Heusch G (2009) Tumor necrosis factor-alpha and its receptors 1 and 2: Yin and Yang in myocardial infarction?

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         description:We previously found that myocardial ischemia/reperfusion (I/R) initiates expression of tumor necrosis factor-α (TNF) leading to coronary endothelial dysfunction. However, it is not clear whether there is a direct relationship between levels of TNF expression and endothelial dysfunction in reperfusion injury. We studied levels of TNF expression by using different transgenic animals expressing varying amounts of TNF in I/R. We crossed TNF overexpression (TNF++/++) with TNF knockout (TNF−/−) mice; thus we have a heterozygote population of mice with the expression of TNF “in between” the TNF−/− and TNF++/++ mice. Mouse hearts were subjected to 30 min of global ischemia followed by 90 min of reperfusion and their vasoactivity before and after I/R was examined in wild type (WT), TNF−/−, TNF++/++ and TNF heterozygote (TNF−/++, cross between TNF−/− and TNF++/++) mice. In heterozygote TNF−/++ mice with intermediate cardiac-specific expression of TNF, acetylcholine-induced or flow-induced endothelial-dependent vasodilation following I/R was between TNF++/++ and TNF−/− following I/R. Neutralizing antibodies to TNF administered immediately before the onset of reperfusion-preserved endothelial-dependent dilation following I/R in WT, TNF−/++ and TNF++/++ mice. In WT, TNF−/++ and TNF++/++ mice, I/R-induced endothelial dysfunction was progressively lessened by administration of free-radical scavenger TEMPOL immediately before initiating reperfusion. During I/R, production of superoxide (O2 ·−) was greatest in TNF++/++ mice as compared to WT, TNF−/++ and TNF−/− mice. Following I/R, arginase mRNA expression was elevated in the WT, substantially elevated in the TNF−/++ and TNF++/++ mice and not affected in the TNF−/− mice. These results suggest that the level of TNF expression determines arginase expression in endothelial cells during myocardial I/R, which is one of the mechanisms by which TNF compromises coronary endothelial function in reperfusion injury.
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