scholarly journals C1q/tumor necrosis factor‐related protein‐3 improves renal fibrosis via inhibiting notch signaling pathways

2019 ◽  
Vol 234 (12) ◽  
pp. 22352-22364
Author(s):  
Xinpan Chen ◽  
Yiru Wu ◽  
Zongli Diao ◽  
Xue Han ◽  
Dishan Li ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Renal Fibrosis ◽  
Tumor Necrosis ◽  
Related Protein ◽  
Necrosis Factor

scholarly journals Roles of TRP14, a Thioredoxin-related Protein in Tumor Necrosis Factor-α Signaling Pathways

2003 ◽  
Vol 279 (5) ◽  
pp. 3151-3159 ◽  
Author(s):  
Woojin Jeong ◽  
Tong-Shin Chang ◽  
Emily S. Boja ◽  
Henry M. Fales ◽  
Sue Goo Rhee
Keyword(s):  
Tumor Necrosis Factor ◽  
Signaling Pathways ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Related Protein ◽  
Factor Α ◽  
Necrosis Factor

Contributions of angiotensin II and tumor necrosis factor-α to the development of renal fibrosis

2001 ◽  
Vol 280 (5) ◽  
pp. F777-F785 ◽  
Author(s):  
Guangjie Guo ◽  
Jeremiah Morrissey ◽  
Ruth McCracken ◽  
Timothy Tolley ◽  
Helen Liapis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Tumor Necrosis Factor ◽  
Renal Fibrosis ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Wild Type ◽  
Tnf Α ◽  
Factor Α ◽  
Tgf Β1 ◽  
Necrosis Factor

Angiotensin II upregulates tumor necrosis factor-α (TNF-α) in the rat kidney with unilateral ureteral obstruction (UUO). In a mouse model of UUO, we found that tubulointerstitial fibrosis is blunted when the TNF-α receptor, TNFR1, is functionally knocked out. In this study, we used mutant mice with UUO in which the angiotensin II receptor AT1a or the TNF-α receptors TNFR1 and TNFR2 were knocked out to elucidate interactions between the two systems. The contribution of both systems to renal fibrosis was assessed by treating TNFR1/TNFR2-double knockout (KO) mice with an angiotensin-converting enzyme inhibitor, enalapril. The increased interstitial volume (Vvint) in the C57BI/6 wild-type mouse was decreased in the AT1a KO from 32.8 ± 4.0 to 21.0 ± 3.7% ( P < 0.005) or in the TNFR1/TNFR2 KO to 22.3 ± 2.1% ( P < 0.005). The Vvint of the TNFR1/TNFR2 KO was further decreased to 15.2 ± 3.7% ( P < 0.01) by enalapril compared with no treatment. The induction of TNF-α mRNA and transforming growth factor-β1 (TGF-β1) mRNA in the kidney with UUO was significantly blunted in the AT1a or TNFR1/TNFR2 KO mice compared with the wild-type mice. Treatment of the TNFR1/TNFR2 KO mouse with enalapril reduced both TNF-α and TGF-β1 mRNA and their proteins to near normal levels. Also, α-smooth muscle actin expression and myofibroblast proliferation were significantly inhibited in the AT1a or TNFR1/TNFR2 KO mice, and they were further inhibited in enalapril-treated TNFR1/TNFR2 KO mice. Incapacitating the angiotensin II or the TNF-α systems individually leads to partial blunting of fibrosis. Incapacitating both systems, by using a combination of genetic and pharmacological means, further inhibited interstitial fibrosis and tubule atrophy in obstructive nephropathy.

scholarly journals Alpha-Lipoic Acid Suppresses Extracellular Histone-Induced Release of the Infammatory Mediator Tumor Necrosis Factor-α by Macrophages

2017 ◽  
Vol 42 (6) ◽  
pp. 2559-2568 ◽  
Author(s):  
Ping Chang ◽  
Juan Liu ◽  
Ying Yu ◽  
Shao-Ye Cui ◽  
Zhen-Hui Guo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Signaling Pathways ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Raw 264.7 ◽  
Alpha Lipoic Acid ◽  
Tnf Α ◽  
Extracellular Histones ◽  
Factor Α ◽  
Necrosis Factor

Background/Aims: This study investigated signaling pathways via which extracellular histones induce the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) release from the macrophage cell line RAW 264.7 and the anti-inflammatory efficacy of the antioxidant alpha-lipoic acid (ALA). Methods: ELISA and western blotting analyses were conducted to detect the release of TNF-α from histone-stimulated RAW 264.7 macrophages and the associated phospho-activation of MAPKs (ERK and p38) and NF-κB p65. The effects of ALA on the release of TNF-α and phospho-activation of the MAPKs and NF-κB p65 were studied. P < 0.05 was considered statistically significant. Results: Extracellular histones dose-dependently induced TNF-α release from RAW 264.7 cells and increased the phosphorylation of p38, ERK, and NF-κB p65. TNF-α release was markedly suppressed by p38, ERK, and NF-kB inhibitors. ALA reduced histone-induced TNF-α release, ERK/p38 MAPK activation, and NF-kB activation without affecting macrophage viability. Conclusion: Histones induce TNF-α release from macrophages by activating the MAPK and NF-kB signaling pathways, while ALA suppresses this response by inhibiting ERK, p38 and NF-kB. These findings identify potentially critical inflammatory signaling pathways in sepsis and molecular targets for sepsis treatment.

117 THE COMPLEMENT c1q TUMOR NECROSIS FACTOR-RELATED PROTEIN 1 LEVEL IN PATIENTS WITH SLEEP APNEA AND PRIMARY ALDSTERONISM

2012 ◽  
Vol 30 ◽  
pp. e36
Author(s):  
Nanfang Li ◽  
Weiping Cheng ◽  
Xiaoguang Yao ◽  
Wanyong Ma ◽  
Zhitao Yan ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Related Protein ◽  
Complement C1q ◽  
Necrosis Factor

scholarly journals GW29-e1323 C1q-tumor necrosis factor-related protein-3 exacerbates cardiac hypertrophy in mice

2018 ◽  
Vol 72 (16) ◽  
pp. C40-C41
Author(s):  
Zhenguo Ma ◽  
Xin Zhang ◽  
Qizhu Tang
Keyword(s):  
Tumor Necrosis Factor ◽  
Cardiac Hypertrophy ◽  
Tumor Necrosis ◽  
Related Protein ◽  
Necrosis Factor

Signaling Pathways Involved in the Stimulation of DNA Synthesis by Tumor Necrosis Factor and Lipopolysaccharide in Chick Embryo Cardiomyocytes

2003 ◽  
pp. 359-371
Author(s):  
Benedetta Tantini ◽  
Carla Pignatti ◽  
Flavio Flamigni ◽  
Claudio Stefanelli ◽  
Monia Fattori ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Chick Embryo ◽  
Dna Synthesis ◽  
Signaling Pathways ◽  
Tumor Necrosis ◽  
Necrosis Factor ◽  
Stimulation Of
Sign in / Sign up

Export Citation Format

Share Document