Decreased Risk for Myocardial Infarction and Lower Tumor Necrosis Factor–α Levels in Carriers of Variants of the PDCD1 Gene

2006 ◽  
Vol 67 (9) ◽  
pp. 700-705 ◽  
Author(s):  
Anna M. Bennet ◽  
Marta Alarcón-Riquelme ◽  
Björn Wiman ◽  
Ulf de Faire ◽  
Ludmila Prokunina-Olsson
Keyword(s):  
Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

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.

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 Myocardial infarction marker levels are influenced by prothrombin and tumor necrosis factor-α gene polymorphisms in young patients

Cytokine ◽  
2013 ◽  
Vol 61 (1) ◽  
pp. 218-222 ◽  
Author(s):  
Loredana Vaccarino ◽  
Silvana Vitale ◽  
Marco Caruso ◽  
Marisa Palmeri ◽  
Letizia Scola ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Young Patients ◽  
Factor Α ◽  
Necrosis Factor
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