scholarly journals High Mobility Group Box 1 Promotes Small Intestinal Damage Induced by Nonsteroidal Anti-Inflammatory Drugs through Toll-Like Receptor 4

2012 ◽  
Vol 181 (1) ◽  
pp. 98-110 ◽  
Author(s):  
Yuji Nadatani ◽  
Toshio Watanabe ◽  
Tetsuya Tanigawa ◽  
Hirohisa Machida ◽  
Hirotoshi Okazaki ◽  
...  
Keyword(s):  
High Mobility ◽  
High Mobility Group ◽  
Intestinal Damage ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Inflammatory Drugs ◽  
Small Intestinal ◽  
Anti Inflammatory

M1849 High-Mobility Group Box-1: A Promoting Factor for Small Intestinal Damage Induced by Nonsteroidal Anti-Inflammatory Drugs

2010 ◽  
Vol 138 (5) ◽  
pp. S-431-S-432
Author(s):  
Yuji Nadatani ◽  
Toshio Watanabe ◽  
Tetsuya Tanigawa ◽  
Fumikazu Ohkawa ◽  
Koji Otani ◽  
...  
Keyword(s):  
High Mobility ◽  
High Mobility Group ◽  
Intestinal Damage ◽  
Inflammatory Drugs ◽  
Small Intestinal ◽  
Anti Inflammatory

Non-steroidal anti-inflammatory drug-induced small intestinal damage is Toll-like receptor 4 dependent

Gut ◽  
2007 ◽  
Vol 57 (2) ◽  
pp. 181-187 ◽  
Author(s):  
T Watanabe ◽  
K Higuchi ◽  
A Kobata ◽  
H Nishio ◽  
T Tanigawa ◽  
...  
Keyword(s):  
Intestinal Damage ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Drug Induced ◽  
Inflammatory Drug ◽  
Small Intestinal ◽  
Anti Inflammatory

scholarly journals TNF-α Activates High-Mobility Group Box 1 - Toll-Like Receptor 4 Signaling Pathway in Human Aortic Endothelial Cells

2016 ◽  
Vol 38 (6) ◽  
pp. 2139-2151 ◽  
Author(s):  
Won Seok Yang ◽  
Nam Jeong Han ◽  
Jin Ju Kim ◽  
Mee Jeong Lee ◽  
Su-Kil Park
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
High Mobility ◽  
Neutralizing Antibody ◽  
High Mobility Group ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Aortic Endothelial Cells ◽  
Tnf Α ◽  
Human Aortic Endothelial Cells

Background/Aims: Toll-like receptor 4 (TLR4) interacts with endogenous substances as well as lipopolysaccharide. We explored whether TLR4 is implicated in tumor necrosis factor-α (TNF-α) signal transduction in human aortic endothelial cells. Methods: The pathway was evaluated by transfection of siRNAs, immunoprecipitation and Western blot analysis. Results: TNF-α activated spleen tyrosine kinase (Syk) within 10 min, which led to endothelin-1 (ET-1) production. TLR4 was also rapidly activated by TNF-α stimulation, as shown by recruitment of interleukin-1 receptor-associated kinase 1 to TLR4 and its adaptor molecule, myeloid differentiation factor 88 (MyD88). siRNA depletion of TLR4 markedly attenuated TNF-α-induced Syk activation and ET-1 production. TLR4 inhibitor (CLI-095), TLR4-neutralizing antibody and siRNA depletion of MyD88 also attenuated TNF-α-induced Syk activation. Syk was co-immunoprecipitated with TLR4, and TNF-α activated Syk bound to TLR4. High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-α stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant. Glycyrrhizin (HMGB1 inhibitor), HMGB1-neutralizing antibody and siRNA depletion of HMGB1 all suppressed TNF-α-induced Syk activation and ET-1 production. Conclusion: Upon TNF-α stimulation, TLR4 is activated by HMGB1 that is immediately released after the generation of reactive oxygen species, and plays a crucial role in the signal transduction.

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