Modulation of PKC signaling and induction of apoptosis through suppression of reactive oxygen species and tumor necrosis factor receptor 1 (TNFR1): key role of quercetin in cancer prevention

Tumor Biology ◽  
2015 ◽  
Vol 36 (11) ◽  
pp. 8913-8924 ◽  
Author(s):  
Akhilendra Kumar Maurya ◽  
Manjula Vinayak
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis Factor ◽  
Cancer Prevention ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Oxygen Species ◽  
Pkc Signaling ◽  
Induction Of Apoptosis ◽  
Necrosis Factor

scholarly journals TNFRSF14 deficiency protects against ovariectomy-induced adipose tissue inflammation

2014 ◽  
Vol 220 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Eun-Kyung Choi ◽  
Woon-Ki Kim ◽  
Ok-Joo Sul ◽  
Yun-Kyung Park ◽  
Eun-Sook Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
Tumor Necrosis ◽  
Ovarian Function ◽  
Tumor Necrosis Factor Receptor ◽  
Oxygen Species ◽  
Adipose Tissue Inflammation ◽  
Metabolic Perturbation ◽  
Necrosis Factor

To elucidate the role of tumor necrosis factor receptor superfamily member 14 (TNFRSF14) in metabolic disturbance due to loss of ovarian function, ovariectomy (OVX) was performed in TNFRSF 14-knockout mice. OVX increased fat mass and infiltration of highly inflammatory CD11c cells in the adipose tissue (AT), which was analyzed by flow cytometry, and resulted in disturbance of glucose metabolism, whereas TNFRSF14 deficiency attenuated these effects. TNFRSF14 deficiency decreased recruitment of CD11c-expressing cells in AT and reduced the polarization of bone marrow-derived macrophages to M1. Upon engagement of LIGHT, a TNFRSF14 ligand, TNFRSF14 enhanced the expression of CD11c via generation of reactive oxygen species, suggesting a role of TNFRSF14 as a redox modulator. TNFRSF14 participated in OVX-induced AT inflammation via upregulation of CD11c, resulting in metabolic perturbation. TNFRSF14 could be used as a therapeutic target for the treatment of postmenopausal syndrome by reducing AT inflammation.

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.

Role of Reactive Oxygen Species in Tumor Necrosis Factor Toxicity

2000 ◽  
pp. 245-264
Author(s):  
Vera Goossens ◽  
Kurt De Vos ◽  
Dominique Vercammen ◽  
Margino Steemans ◽  
Katia Vancompernolle ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor (TNF)-α-induced IL-8 expression in gastric epithelial cells: Role of reactive oxygen species and AP endonuclease-1/redox factor (Ref)-1

Cytokine ◽  
2009 ◽  
Vol 46 (3) ◽  
pp. 359-369 ◽  
Author(s):  
Ann M. O’Hara ◽  
Asima Bhattacharyya ◽  
Jie Bai ◽  
Randy C. Mifflin ◽  
Peter B. Ernst ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Oxygen Species ◽  
Gastric Epithelial Cells ◽  
Ap Endonuclease ◽  
Tnf Α ◽  
Necrosis Factor

scholarly journals Role of Reactive Oxygen Species in Tumor Necrosis Factor-alpha Induced Endothelial Dysfunction

2008 ◽  
Vol 4 (4) ◽  
pp. 245-255 ◽  
Author(s):  
Xiuping Chen ◽  
Bradley Andresen ◽  
Michael Hill ◽  
Jing Zhang ◽  
Frank Booth ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Oxygen Species ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

The Role of the Tumor Necrosis Factor Receptor in 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-Induced Colitis in Mice

2005 ◽  
Vol 50 (9) ◽  
pp. 1669-1676 ◽  
Author(s):  
Minoru Nakai ◽  
Kaori Sudo ◽  
Yasuhiro Yamada ◽  
Yasushi Kojima ◽  
Tomohiro Kato ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Sulfonic Acid ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Trinitrobenzene Sulfonic Acid ◽  
Necrosis Factor
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