High mobility group box 1 promotes small intestinal damage induced by nonsteroidal anti-inflammatory drugs through Toll-like receptor 4.

[1]  P. Vandenabeele,et al.  Severity of doxorubicin‐induced small intestinal mucositis is regulated by the TLR‐2 and TLR‐9 pathways , 2012, The Journal of pathology.

[2]  K. Tominaga,et al.  Mitochondrial disorders in NSAIDs-induced small bowel injury , 2011, Journal of clinical biochemistry and nutrition.

[3]  T. Misteli,et al.  Erratum: Release of chromatin protein HMGB1 by necrotic cells triggers inflammation (Nature (2002) 418 (191-195)) , 2010 .

[4]  J. Wang,et al.  Extracellular High Mobility Group Box-1 (HMGB1) Inhibits Enterocyte Migration via Activation of Toll-like Receptor-4 and Increased Cell-Matrix Adhesiveness* , 2009, The Journal of Biological Chemistry.

[5]  K. Tominaga,et al.  Probiotic Lactobacillus casei strain Shirota prevents indomethacin-induced small intestinal injury: involvement of lactic acid. , 2009, American journal of physiology. Gastrointestinal and liver physiology.

[6]  A. Sepulveda,et al.  Ethyl pyruvate decreases HMGB1 release and ameliorates murine colitis , 2009, Journal of leukocyte biology.

[7]  L. Lindgren,et al.  Bile high-mobility group box 1 contributes to gut barrier dysfunction in experimental endotoxemia. , 2009, American journal of physiology. Regulatory, integrative and comparative physiology.

[8]  Toshio Watanabe,et al.  Present status and strategy of NSAIDs-induced small bowel injury , 2009, Journal of Gastroenterology.

[9]  K. Tominaga,et al.  Small bowel injury by low-dose enteric-coated aspirin and treatment with misoprostol: a pilot study. , 2008, Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.

[10]  B. Funke,et al.  High-Mobility Group Box-1 in Ischemia-Reperfusion Injury of the Heart , 2008, Circulation.

[11]  Jeon-Soo Shin,et al.  High Mobility Group Box 1 Protein Binding to Lipopolysaccharide Facilitates Transfer of Lipopolysaccharide to CD14 and Enhances Lipopolysaccharide-Mediated TNF-α Production in Human Monocytes1 , 2008, The Journal of Immunology.

[12]  S. Chadban,et al.  TLR4 activation mediates kidney ischemia/reperfusion injury. , 2007, The Journal of clinical investigation.

[13]  M. Omata,et al.  Essential roles of high-mobility group box 1 in the development of murine colitis and colitis-associated cancer. , 2007, Biochemical and biophysical research communications.

[14]  K. Tominaga,et al.  Non-steroidal anti-inflammatory drug-induced small intestinal damage is Toll-like receptor 4 dependent , 2007, Gut.

[15]  Y. Takeyama,et al.  Blockade of high mobility group box-1 protein attenuates experimental severe acute pancreatitis. , 2006, World journal of gastroenterology.

[16]  Masayoshi Takeuchi,et al.  RAGE Control of Diabetic Nephropathy in a Mouse Model , 2006, Diabetes.

[17]  K. Tracey,et al.  HMGB1 SIGNALS THROUGH TOLL-LIKE RECEPTOR (TLR) 4 AND TLR2 , 2006, Shock.

[18]  R. Pieters,et al.  Contributions of mucosal immune cells to methotrexate-induced mucositis. , 2006, International immunology.

[19]  M. Presta,et al.  Cutting Edge: Extracellular High Mobility Group Box-1 Protein Is a Proangiogenic Cytokine1 , 2006, The Journal of Immunology.

[20]  Hiroshi Yamamoto,et al.  The N-terminal domain of thrombomodulin sequesters high-mobility group-B1 protein, a novel antiinflammatory mechanism. , 2005, The Journal of clinical investigation.

[21]  I. Douglas,et al.  HMGB1 contributes to the development of acute lung injury after hemorrhage. , 2005, American journal of physiology. Lung cellular and molecular physiology.

[22]  C. Esmon Do-all receptor takes on coagulation, inflammation , 2005, Nature Medicine.

[23]  K. Tracey,et al.  The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion , 2005, The Journal of experimental medicine.

[24]  R. McIntyre,et al.  Hemorrhage-induced acute lung injury is TLR-4 dependent. , 2004, American journal of physiology. Regulatory, integrative and comparative physiology.

[25]  E. Schleicher,et al.  Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response. , 2004, The Journal of clinical investigation.

[26]  E. Abraham,et al.  Involvement of Toll-like Receptors 2 and 4 in Cellular Activation by High Mobility Group Box 1 Protein* , 2004, Journal of Biological Chemistry.

[27]  J. Emond,et al.  Blockade of receptor for advanced glycation end product (RAGE) attenuates ischemia and reperfusion injury to the liver in mice , 2004, Hepatology.

[28]  K. Tracey,et al.  Activation of gene expression in human neutrophils by high mobility group box 1 protein. , 2003, American journal of physiology. Cell physiology.

[29]  Michael Bustin,et al.  Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells. , 2003, Blood.

[30]  M. J. Cody,et al.  Induction of In Vitro Reprogramming by Toll-Like Receptor (TLR)2 and TLR4 Agonists in Murine Macrophages: Effects of TLR “Homotolerance” Versus “Heterotolerance” on NF-κB Signaling Pathway Components1 , 2003, The Journal of Immunology.

[31]  K. Tracey,et al.  Ethyl pyruvate prevents lethality in mice with established lethal sepsis and systemic inflammation , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[32]  K. Tracey,et al.  HMGB1 B box increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice. , 2002, Gastroenterology.

[33]  S. Müller,et al.  The High Mobility Group (Hmg) Boxes of the Nuclear Protein Hmg1 Induce Chemotaxis and Cytoskeleton Reorganization in Rat Smooth Muscle Cells , 2001, The Journal of cell biology.

[34]  K. Tracey,et al.  High Mobility Group 1 Protein (Hmg-1) Stimulates Proinflammatory Cytokine Synthesis in Human Monocytes , 2000, The Journal of experimental medicine.

[35]  T. Kislinger,et al.  Blockade of RAGE–amphoterin signalling suppresses tumour growth and metastases , 2000, Nature.

[36]  Michael Bustin,et al.  Regulation of DNA-Dependent Activities by the Functional Motifs of the High-Mobility-Group Chromosomal Proteins , 1999, Molecular and Cellular Biology.

[37]  K. Tracey,et al.  HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.

[38]  S. Akira,et al.  Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. , 1999, Journal of immunology.

[39]  T. Misteli,et al.  Release of chromatin protein HMGB1 by necrotic cells triggers inflammation , 2010, Nature.

[40]  杉森 聖司 Evaluation of small bowel injury in patients with rheumatoid arthritis by capsule endoscopy : effects of anti-rheumatoid arthritis drugs , 2010 .

[41]  S. Chiou,et al.  Survivin: a novel target for indomethacin-induced gastric injury. , 2005, Gastroenterology.

[42]  D. Graham,et al.  Visible small-intestinal mucosal injury in chronic NSAID users. , 2005, Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.