scholarly journals Quercetin enhances apoptotic effect of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer‐binding protein homologous protein (CHOP)‐death receptor 5 pathway

2014 ◽  
Vol 105 (5) ◽  
pp. 520-527 ◽  
Author(s):  
Liu Yi ◽  
Yang Zongyuan ◽  
Gong Cheng ◽  
Zhang Lingyun ◽  
Yu GuiLian ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis ◽  
Death Receptor ◽  
Ovarian Cancer Cells ◽  
Oxygen Species ◽  
Death Receptor 5 ◽  
Homologous Protein ◽  
Enhancer Binding Protein ◽  
Apoptotic Effect ◽  
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.

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