Tumor Necrosis Factor-Alpha and Inflammation-Mediated Cardiac Injury

Howerton, Edna; Tarzami, Sima T.

doi:10.4172/2157-7013.1000268

Cited by 7 publications

(6 citation statements)

References 50 publications

(55 reference statements)

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“…However, TNFR2 induces an anti-inflammatory effect to counter the effects of TNFR1 on tissue repair. In the clinic, TNF-α levels are known to increase and TNF-α receptors are known to significantly decrease in patients with chronic heart failure [ 46 ]. Therefore, variations in TNFR1 and TNFR2 signaling and regulation during cardiac disorders remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Etanercept Ameliorates Cardiac Fibrosis in Rats with Diet-Induced Obesity

Hsu

et al. 2021

Pharmaceuticals

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Diet-induced obesity (DIO) is considered the main risk factor for cardiovascular diseases. Increases in the plasma levels of tumor necrosis factor alpha (TNF-α) is associated with DIO. Etanercept, a TNF-α inhibitor, has been shown to alleviate cardiac hypertrophy. To investigate the effect of etanercept on cardiac fibrosis in DIO model, rats on high fat diet (HFD) were subdivided into two groups: the etanercept group and vehicle group. Cardiac injury was identified by classic methods, while fibrosis was characterized by histological analysis of the hearts. Etanercept treatment at 0.8 mg/kg/week twice weekly by subcutaneous injection effectively alleviates the cardiac fibrosis in HFD-fed rats. STAT3 activation seems to be induced in parallel with fibrosis-related gene expression in the hearts of HFD-fed rats. Decreased STAT3 activation plays a role in the etanercept-treated animals. Moreover, fibrosis-related genes are activated by palmitate in parallel with STAT3 activation in H9c2 cells. Etanercept may inhibit the effects of palmitate, but it is less effective than a direct inhibitor of STAT3. Direct inhibition of STAT3 activation by etanercept seems unlikely. Etanercept has the ability to ameliorate cardiac fibrosis through reduction of STAT3 activation after the inhibition of TNF-α and/or its receptor.

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Section: Discussionmentioning

confidence: 99%

Etanercept Ameliorates Cardiac Fibrosis in Rats with Diet-Induced Obesity

Hsu

et al. 2021

Pharmaceuticals

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“…The results of present study shows that a significant increase in serum level of IL-8, MCP-1 and TNF-α observed during the infection with E. histolytica, which reflect a pro-inflammatory role of these cytokines in the infection [13,14,15]. Trophozoite attachment to host epithelial and inflammatory cells and to colonic mucins and bacteria is mediated by a lectin specific for galactose/N-acetyl-galactosamine [16,17,18].…”

Section: Discussionmentioning

confidence: 50%

Serum level of Interleukin (IL)-8, Monocyte Chemoattractant Protein (MCP)-1 and Tumor Necrosis Factor (TNF)-α in children infected with Entamoeba histolytica

Ahmed¹,

Al-Nasiri²

2019

Tikrit J. Pure Sci.

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Entamoeba histolytica is an enteric protozoan parasite which caused tissue invasive amoebiasis. It can induce the production of cytokines (such as IL-8 and TNF-α) and chemokines (such as MCP-1) from intestinal epithelial cells. This study was done to detect the serum level of IL-8, MCP-1 and TNF-α, using an enzyme-linked immunosorbent assay, in 60 children affected by amoebiasis to correlate the production of these cytokines with infection and comparison with the healthy persons (n= 30). Three aged groups (1 month- 2 year, 2-4 year and 4-6 year) were entered in the study for patients and healthy controls. The level of IL-8 (37.22 ± 7.06, 37.35 ± 1.981 and 36.45 ± 4.39 pg/ml) in children with amoebiasis were higher significantly compared with the level in healthy children (29.95 ± 4.30, 26.90 ± 4.17 and 25.32 ± 2.31 pg/ml) in all age groups (1 month- 2 year, 2-4 year and 4-6 year, respectively). Significant differences in the level of MCP-1 which were higher (28.92 ± 1.48, 30.85 ± 3.78 and 31.91 ± 6.82 pg/ml) in children with amoebiasis than in healthy children (18.44 ± 0.74, 22.62 ± 6.25 and 18.30 ± 1.43 pg/ml) in all age groups (respectively). Also, the level of TNF-α were higher significantly (58.05 ± 6.90, 55.87 ± 3.81 and 57.32 ± 8.86 pg/ml) in children with amoebiasis compared with healthy children (42.91 ± 2.54, 43.54 ± 3.42 and 42.64 ± 3.47 pg/ml, respectively) in all age groups (respectively). These findings reflect a role of IL-8, MCP-1 and TNF-α in E. histolytica infection.

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“…Thus, TNF-α has been used for malignant disease treatment since beginning of the twentieth century. Ever since the discovery of TNF-α, it has been comprehensively studied for its involvement in acute and chronic inflammation, cell differentiation and proliferation, stimulation of programs of cellular suicide including apoptosis and necroptosis, cell metabolism, autoimmune diseases and cancer [ 1 , 2 , 3 , 4 , 5 ].…”

Section: Discussionmentioning

confidence: 99%

“…It is involved in host defense against microbial infections, control of cell survival and proliferation and efficient antitumor activities. It is also called cachectin, endotoxin-induced factor in serum, or differentiation-inducing factor [ 3 , 4 , 5 ]. This cytokine is secreted from activated macrophages, monocytes and natural killer (NK) cells in response to any immunological challenge [ 2 , 6 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

A De Novo Optimized Cell-Free System for the Expression of Soluble and Active Human Tumor Necrosis Factor-Alpha

El-Baky

El‐Fakharany

Sabry

et al. 2022

Biology

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Cell-free (in vitro) expression is a robust alternative platform to the cell-based (in vivo) system for recombinant protein production. Tumor necrosis factor-alpha (TNF-α) is an effective pro-inflammatory cytokine with pleiotropic effects. The aim of the current study was de novo optimized expression of soluble and active human TNF-α by an in vitro method in an E. coli-based cell-free protein synthesis (CFPS) system and its biological activity evaluation. The codon-optimized synthetic human TNF-α gene was constructed by a two-step PCR, cloned into pET101/D-TOPO vector and then expressed by the E. coli CFPS system. Cell-free expression of the soluble protein was optimized using a response surface methodology (RSM). The anticancer activity of purified human TNF-α was assessed against three human cancer cell lines: Caco-2, HepG-2 and MCF-7. Data from RSM revealed that the lowest value (7.2 µg/mL) of cell-free production of recombinant human TNF-α (rhTNF-α) was obtained at a certain incubation time (6 h) and incubation temperature (20 °C), while the highest value (350 µg/mL) was recorded at 4 h and 35 °C. This rhTNF-α showed a significant anticancer potency. Our findings suggest a cell-free expression system as an alternative platform for producing soluble and functionally active recombinant TNF-α for further research and clinical trials.

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Tumor Necrosis Factor-Alpha and Inflammation-Mediated Cardiac Injury

Cited by 7 publications

References 50 publications

Etanercept Ameliorates Cardiac Fibrosis in Rats with Diet-Induced Obesity

Etanercept Ameliorates Cardiac Fibrosis in Rats with Diet-Induced Obesity

Serum level of Interleukin (IL)-8, Monocyte Chemoattractant Protein (MCP)-1 and Tumor Necrosis Factor (TNF)-α in children infected with Entamoeba histolytica

A De Novo Optimized Cell-Free System for the Expression of Soluble and Active Human Tumor Necrosis Factor-Alpha

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