scholarly journals Suppression of tumor necrosis factor receptor-associated protein 1 expression induces inhibition of cell proliferation and tumor growth in human esophageal cancer cells

FEBS Journal ◽  
2014 ◽  
Vol 281 (12) ◽  
pp. 2805-2819 ◽  
Author(s):  
Xin Tian ◽  
Ping Ma ◽  
Cheng-Guang Sui ◽  
Fan-Dong Meng ◽  
Yan Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Associated Protein ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells ◽  
Necrosis Factor

MO071PROTEINS LINKED TO ATHEROSCLEROSIS AND CELL PROLIFERATION ARE ASSOCIATED WITH SHRUNKEN PORE SYNDROME IN HEART FAILURE PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Liana Xhakollari ◽  
Amra Jujic ◽  
John Molvin ◽  
Peter M Nilsson ◽  
Hannes Holm ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Proliferation ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Scavenger Receptor ◽  
Interleukin 2 ◽  
Tumor Necrosis Factor Receptor ◽  
Heart Failure Patients ◽  
Cardiovascular Morbidity And Mortality ◽  
Necrosis Factor

Abstract Background and Aims The “Shrunken pore syndrome” is characterized by a difference in renal filtration between cystatin C and creatinine resulting in a low eGFRcystatinC/eGFRcreatinine-ratio, and studies have demonstrated a high risk for cardiovascular morbidity and mortality for patients with shrunken pore syndrome. In this observational study, we explored associations between shrunken pore syndrome and proteins implicated in cardiovascular disease and inflammation in patients with heart failure. Method Plasma samples from 300 individuals HARVEST-Malmö trial hospitalized for the diagnosis of heart failure (mean age 75 years; 30% female), were analyzed with a proximity extension assay consisting of 92 proteins, to identify proteins associated with shrunken pore syndrome. Shrunken pore syndrome was defined as eGFRcystatinC ≤60% of eGFRcreatinine. Proteins associated with shrunken pore syndrome in the initial age and sex-adjusted analyses (Bonferroni-corrected p≤ 5.4x10-4) were further adjusted for relevant covariates. Results In multivariate analyses, Shrunken pore syndrome was associated with elevated levels of six proteins; scavenger receptor cysteine-rich type 1 protein M130, tumor necrosis factor receptor 1, tumor necrosis factor receptor 2, osteoprotegerin, interleukin-2 receptor subunit alpha, and tyrosine-protein kinase receptor UFO (p<0.05). Conclusion In heart failure patients, shrunken pore syndrome was independently associated with proteins linked to atherosclerosis and cell proliferation.

Tumor Necrosis Factor Receptor-Associated Factor 5 Promotes Arterial Neointima Formation through Smooth Muscle Cell Proliferation

2019 ◽  
Vol 56 (6) ◽  
pp. 308-319
Author(s):  
Florian Willecke ◽  
Benjamin Rupprecht ◽  
Mark Colin Gissler ◽  
Katharina Pfeiffer ◽  
Nathaly Anto-Michel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Smooth Muscle Cell Proliferation ◽  
Neointima Formation ◽  
Necrosis Factor

scholarly journals Involvement of Tumor Necrosis Factor Receptor-associated Protein 1 (TRAP1) in Apoptosis Induced by β-Hydroxyisovalerylshikonin

2004 ◽  
Vol 279 (41) ◽  
pp. 42503-42515 ◽  
Author(s):  
Yutaka Masuda ◽  
Genryu Shima ◽  
Toshihiro Aiuchi ◽  
Masayo Horie ◽  
Kouichi Hori ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Associated Protein ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit II

2019 ◽  
Vol 7 ◽  
Author(s):  
Fei Xiang ◽  
Si-yuan Ma ◽  
Yan-ling Lv ◽  
Dong-xia Zhang ◽  
Hua-pei Song ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis Factor ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Cardiomyocyte Apoptosis ◽  
Oxygen Species ◽  
Receptor Associated Protein ◽  
Necrosis Factor

Abstract Background Tumor necrosis factor receptor-associated protein 1 (TRAP1) plays a protective effect in hypoxic cardiomyocytes, but the precise mechanisms are not well clarified. The study is aimed to identify the mechanism of TRAP1 on hypoxic damage in cardiomyocytes. Methods In this study, the effects of TRAP1 and cytochrome c oxidase subunit II (COXII) on apoptosis in hypoxia-induced cardiomyocytes were explored using overexpression and knockdown methods separately. Results Hypoxia induced cardiomyocyte apoptosis, and TRAP1 overexpression notably inhibited apoptosis induced by hypoxia. Conversely, TRAP1 silencing promoted apoptosis in hypoxic cardiomyocytes. Further investigation revealed that the proapoptotic effects caused by the silencing of TRAP1 were prevented by COXII overexpression, whereas COXII knockdown reduced the antiapoptotic function induced by TRAP1 overexpression. Additionally, changes in the release of cytochrome c from mitochondria into the cytosol and the caspase-3 activity in the cytoplasm, as well as reactive oxygen species production, were found to be correlated with the changes in apoptosis. Conclusions The current study uncovered that TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis through a mitochondria-dependent apoptotic pathway mediated by COXII, in which reactive oxygen species presents as an important component.

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