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

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.

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

Mediators of Inflammation ◽

10.1155/2011/565238 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 10

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.

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Tumor necrosis factor-α: investigation of gene polymorphism and regulation of TACE–TNF-α system in patients with acute myocardial infarction

Molecular Biology Reports ◽

10.1007/s11033-010-0641-x ◽

2010 ◽

Vol 38 (8) ◽

pp. 4971-4977 ◽

Cited By ~ 13

Author(s):

Sayyed Mohammad Hossein Ghaderian ◽

Reza Akbarzadeh Najar ◽

Akram Sadat Tabatabaei Panah

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Tumor Necrosis Factor ◽

Gene Polymorphism ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

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Tumor Necrosis Factor α Regulates Responses to Nerve Growth Factor, Promoting Neural Cell Survival but Suppressing Differentiation of Neuroblastoma Cells

Molecular Biology of the Cell ◽

10.1091/mbc.e07-06-0624 ◽

2008 ◽

Vol 19 (3) ◽

pp. 855-864 ◽

Cited By ~ 21

Author(s):

Yoshinori Takei ◽

Ronald Laskey

Keyword(s):

Nerve Growth Factor ◽

Growth Factor ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Neuroblastoma Cells ◽

Erk Activation ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

Although nerve growth factor (NGF) promotes survival of neurons, tumor necrosis factor α (TNF-α) contributes to cell death triggered by NGF depletion, through TNF-α receptor (TNFR) 1. In contrast to this effect, TNF-α can promote neural cell survival via TNF-α receptor TNFR2. Although these findings demonstrate pivotal roles of TNF-α and NGF in cell fate decisions, cross-talk between these signaling pathways has not been clarified. We find that NGF can induce TNF-α synthesis through the nuclear factor-κB transcription factor. This provides a new basis for examining the cross-talk between NGF and TNF-α. Inhibition of TNFR2 shows opposite effects on two downstream kinases of NGF, extracellular signal-regulated kinase (Erk) and Akt. It increases Erk activation by NGF, and this increased activation induces differentiation of neuroblastoma cell lines. Reciprocally, inhibition of TNFR2 decreases Akt activation by NGF. Consistent with an essential role of Akt in survival signaling, inhibition of TNF-α signaling decreases NGF-dependent survival of neurons from rat dorsal root ganglia. Thus, NGF and NGF-induced TNF-α cooperate to activate Akt, promoting survival of normal neural cells. However, the NGF-induced TNF-α suppresses Erk activation by NGF, blocking NGF-induced differentiation of neuroblastoma cells. TNFR2 signaling could be a novel target to modulate cell responses to NGF.

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