Mn-superoxide dismutase in patients with acute myocardial infarction: Serum appearance and induction by tumor necrosis factor-α

1992 ◽  
Vol 24 ◽  
pp. 167
Author(s):  
Keiichiro Suzuki ◽  
Tsunehiko Kuzuya ◽  
Michihiko Tada ◽  
Naoyuki Taniguchi
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor Necrosis Factor- α at Acute Myocardial Infarction in Rats andÈEffects on Cardiac Fibroblasts

1999 ◽  
Vol 31 (11) ◽  
pp. 1949-1959 ◽  
Author(s):  
Martina Jacobs ◽  
Sibylle Staufenberger ◽  
Ulrich Gergs ◽  
Karsten Meuter ◽  
Katja Brandstätter ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cardiac Fibroblasts ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Effect of Tumor Necrosis Factor-α on Neutralization of Ventricular Fibrillation in Rats with Acute Myocardial Infarction

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Yu Chen ◽  
Qing Zhang ◽  
Yu-Hua Liao ◽  
Zhe Cao ◽  
Yi-Mei Du ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Time Windows ◽  
Border Zone ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The purpose of this study was to explore the effects of tumor necrosis factor-α (TNF-α) on ventricular fibrillation (VF) in rats with acute myocardial infarction (AMI). Rats were randomly classified into AMI group, sham operation group and recombinant human tumor necrosis factor receptor:Fc fusion protein (rhTNFR:Fc) group. Spontaneous and induced VFs were recorded. Monophasic action potentials (MAPs) among different zones of myocardium were recorded at eight time points before and after ligation and MAP duration dispersions (MAPDds) were calculated. Then expression of TNF-α among different myocardial zones was detected. After ligation of the left anterior descending coronary artery, total TNF-α expression in AMI group began to markedly increase at 10 min, reached a climax at 20–30min, and then gradually decreased. The time-windows of VFs and MAPDds in the border zone performed in a similar way. At the same time-point, the expression of TNF-α in the ischemia zone was greater than that in the border zone, and little in the non-ischemia zone. Although the time windows of TNF-α expression, the MAPDds in the border zone and the occurrence of VFs in the rhTNFR:Fc group were similar to those in the AMI group, they all decreased in the rhTNFR:Fc group. Our findings demonstrate that TNF-α could enlarge the MAPDds in the border zone, and promote the onset of VFs.

scholarly journals Measurement of Hepatocyte Growth Factor, Interleukin 6 and Tumor necrosis factor α in Acute Myocardial Infarction

2019 ◽  
Vol 16 (1) ◽  
pp. 33-37
Author(s):  
Asadallah Keshmiri ◽  
Ali Reza Derakhshan ◽  
Afsoon Fazlinejad ◽  
Reza Farid-Hosseini
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Hepatocyte Growth ◽  
Necrosis Factor

Background: Early mortality rate due to acute myocardial infarction (AMI) is approximately 30%, and half of these deaths occur before reaching a hospital. The prevention and early detection play a key role in reducing mortality in AMI. Hepatocyte Growth Factor (HGF), Interleukin 6 (IL-6), and Tumor Necrosis Factor α (TNF-α) are most recent prognostic biomarkers for AMI. The present study was aimed to evaluate the level of these cytokines in AMI. Methods: In this case control study, 39 patients with AMI were compared with 30 healthy subjects. Age, sex and other possible confounding factors were matched. AMI diagnosis was confirmed by typical symptoms, electrocardiogram changes and serum concentration of troponin I and creatine kinase-MB. The levels of TNF-α, IL-6 an HGF at baseline and 3 and 7 days later were measured using ELISA method. Results: Levels of IL-6, TNF-α and HGF increased over time after AMI with ST-segment elevation in study group. The baseline IL-6 levels in AMI group were significantly higher than control group (P<0.05). Conclusions: The results of this study suggest that baseline levels of IL-6 as well as serial changes of serum IL-6, TNF-α and HGF concentrations can be used as potential diagnostic biomarkers in AMI.

scholarly journals Targeted Deletion of Class A Macrophage Scavenger Receptor Increases the Risk of Cardiac Rupture After Experimental Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1904-1911 ◽  
Author(s):  
Kenichi Tsujita ◽  
Koichi Kaikita ◽  
Takanori Hayasaki ◽  
Tsuyoshi Honda ◽  
Hironori Kobayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Experimental Myocardial Infarction ◽  
Cardiac Rupture ◽  
Infarcted Myocardium ◽  
Factor Α ◽  
Necrosis Factor

Background— Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A–deficient (SR-A −/− ) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Methods and Results— Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A −/− and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A −/− mice than in WT mice ( P =0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A −/− mice and 12% (6 of 51 mice) in WT mice ( P =0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A −/− mice compared with WT mice. Real-time reverse transcription–polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A −/− mice compared with WT mice. Furthermore, SR-A −/− mice showed augmented expression of tumor necrosis factor-α and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-α and decreased interleukin-10 expression in activated SR-A −/− macrophages. Conclusions— The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-α and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

The effect of tumor necrosis factor-α on human malignant glial cells

1992 ◽  
Vol 76 (4) ◽  
pp. 652-659 ◽  
Author(s):  
Rolando F. Del Maestro ◽  
Monica Lopez-Torres ◽  
Warren B. McDonald ◽  
Eric C. Stroude ◽  
Indrasen S. Vaithilingam
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis ◽  
Manganese Superoxide Dismutase ◽  
Tumor Necrosis Factor Α ◽  
Superoxide Dismutase Activity ◽  
Manganese Superoxide ◽  
Factor Α ◽  
Necrosis Factor

✓ The influence of human recombinant tumor necrosis factor-α has been assessed on a cell line (U-251) derived from a human malignant glial tumor. The results of this study demonstrate that tumor necrosis factor-α at doses of 50 and 100 ng/ml: 1) did not have cytotoxic or cytostatic effects on the U-251 cell line; 2) significantly increased the intracellular activity of manganese superoxide dismutase but had no effect on copper and zinc superoxide dismutase, catalase, or glutathione peroxidase activity; and 3) did not significantly alter the intracellular or extracellular general protease and collagenase type IV activity of these cells. The resistance of the U-251 cell line to tumor necrosis factor-α cytotoxicity may be related in part to the high intrinsic manganese superoxide dismutase activity present in this cell line combined with the ability of this cell line to induce substantial amounts of protective manganese superoxide dismutase activity in response to tumor necrosis factor-α.

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