HMGB1 induces human lung endothelial cell cytoskeletal rearrangement and barrier disruption.
暂无分享,去创建一个
[1] U. Moens,et al. Heat shock protein 27 phosphorylation: kinases, phosphatases, functions and pathology , 2009, Cellular and Molecular Life Sciences.
[2] R. Lal,et al. Endothelial permeability is controlled by spatially defined cytoskeletal mechanics: atomic force microscopy force mapping of pulmonary endothelial monolayer. , 2009, Nanomedicine : nanotechnology, biology, and medicine.
[3] T. Billiar,et al. HMGB1: Endogenous Danger Signaling , 2008, Molecular medicine.
[4] F. Hou,et al. Advanced glycation end products induce actin rearrangement and subsequent hyperpermeability of endothelial cells THIS ARTICLE HAS BEEN RETRACTED , 2006, APMIS : acta pathologica, microbiologica, et immunologica Scandinavica.
[5] M. Fink,et al. The role of RAGE in the pathogenesis of intestinal barrier dysfunction after hemorrhagic shock. , 2006, American journal of physiology. Gastrointestinal and liver physiology.
[6] K. Tracey,et al. HMGB1 SIGNALS THROUGH TOLL-LIKE RECEPTOR (TLR) 4 AND TLR2 , 2006, Shock.
[7] L. Ware. Pathophysiology of acute lung injury and the acute respiratory distress syndrome. , 2006, Seminars in respiratory and critical care medicine.
[8] E. Abraham,et al. High mobility group box 1 protein interacts with multiple Toll-like receptors. , 2006, American journal of physiology. Cell physiology.
[9] M. Gaestel,et al. MAPKAP kinases — MKs — two's company, three's a crowd , 2006, Nature Reviews Molecular Cell Biology.
[10] M. Presta,et al. Cutting Edge: Extracellular High Mobility Group Box-1 Protein Is a Proangiogenic Cytokine1 , 2006, The Journal of Immunology.
[11] D. Stern,et al. Understanding RAGE, the receptor for advanced glycation end products , 2005, Journal of Molecular Medicine.
[12] Feng Liu,et al. MAP kinases in lung endothelial permeability induced by microtubule disassembly. , 2005, American journal of physiology. Lung cellular and molecular physiology.
[13] 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.
[14] P. Rogalla,et al. Angiogenetic signaling through hypoxia: HMGB1: an angiogenetic switch molecule. , 2005, The American journal of pathology.
[15] K. Tracey,et al. Persistent elevation of high mobility group box-1 protein (HMGB1) in patients with severe sepsis and septic shock* , 2005, Critical care medicine.
[16] U. Andersson,et al. RAGE is the Major Receptor for the Proinflammatory Activity of HMGB1 in Rodent Macrophages , 2005, Scandinavian journal of immunology.
[17] Masaki Tanaka,et al. Contributions of high mobility group box protein in experimental and clinical acute lung injury. , 2004, American journal of respiratory and critical care medicine.
[18] 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.
[19] M. Bryckaert,et al. Control of actin dynamics by p38 MAP kinase – Hsp27 distribution in the lamellipodium of smooth muscle cells , 2004, Journal of Cell Science.
[20] 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.
[21] M. Bianchi,et al. Extracellular HMGB1, a signal of tissue damage, induces mesoangioblast migration and proliferation , 2004, The Journal of cell biology.
[22] M. Welsh,et al. Endothelial barrier dysfunction caused by LPS correlates with phosphorylation of HSP27in vivo , 2004, Cell Biology and Toxicology.
[23] J. Palmblad,et al. High mobility group 1 B‐box mediates activation of human endothelium , 2003, Journal of internal medicine.
[24] J. Garcia,et al. Role of sphingosine-1 phosphate in the enhancement of endothelial barrier integrity by platelet-released products. , 2003, American journal of physiology. Lung cellular and molecular physiology.
[25] Michael Bustin,et al. Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells. , 2003, Blood.
[26] 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.
[27] K. Tracey,et al. HMGB1 B box increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice. , 2002, Gastroenterology.
[28] F. Liu,et al. Critical involvement of p38 MAP kinase in pertussis toxin‐induced cytoskeletal reorganization and lung permeability , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[29] A. Arrigo,et al. Actin cytoskeleton and small heat shock proteins: how do they interact? , 2002, Cell stress & chaperones.
[30] K. Otero,et al. Albumin-derived advanced glycation end-products trigger the disruption of the vascular endothelial cadherin complex in cultured human and murine endothelial cells. , 2001, The Biochemical journal.
[31] S. Dudek,et al. Cytoskeletal regulation of pulmonary vascular permeability. , 2001, Journal of applied physiology.
[32] A. Verin,et al. Sphingosine 1-phosphate promotes endothelial cell barrier integrity by Edg-dependent cytoskeletal rearrangement. , 2001, The Journal of clinical investigation.
[33] K. Tracey,et al. High Mobility Group 1 Protein (Hmg-1) Stimulates Proinflammatory Cytokine Synthesis in Human Monocytes , 2000, The Journal of experimental medicine.
[34] K. Tracey,et al. HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.
[35] C. Manthey,et al. Differential expression and activation of p38 mitogen-activated protein kinase alpha, beta, gamma, and delta in inflammatory cell lineages. , 1999, Journal of immunology.
[36] J. Landry,et al. Oxidative stress-induced actin reorganization mediated by the p38 mitogen-activated protein kinase/heat shock protein 27 pathway in vascular endothelial cells. , 1997, Circulation research.
[37] J. Landry,et al. Modulation of cellular thermoresistance and actin filament stability accompanies phosphorylation-induced changes in the oligomeric structure of heat shock protein 27 , 1995, Molecular and cellular biology.
[38] S. Suter,et al. High bronchoalveolar levels of tumor necrosis factor and its inhibitors, interleukin-1, interferon, and elastase, in patients with adult respiratory distress syndrome after trauma, shock, or sepsis. , 1992, The American review of respiratory disease.
[39] M. Mendelsohn,et al. The 29-kDa proteins phosphorylated in thrombin-activated human platelets are forms of the estrogen receptor-related 27-kDa heat shock protein. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[40] A. Fowler,et al. Tumor necrosis factor levels in serum and bronchoalveolar lavage fluid of patients with the adult respiratory distress syndrome. , 1991, The American review of respiratory disease.
[41] A. Arrigo. Tumor necrosis factor induces the rapid phosphorylation of the mammalian heat shock protein hsp28 , 1990, Molecular and cellular biology.
[42] M. Singer,et al. TUMOUR NECROSIS FACTOR IN BRONCHOPULMONARY SECRETIONS OF PATIENTS WITH ADULT RESPIRATORY DISTRESS SYNDROME , 1989, The Lancet.
[43] A. Malik,et al. Phallacidin prevents thrombin-induced increases in endothelial permeability to albumin. , 1989, The American journal of physiology.
[44] M. Morrell,et al. ABSORPTION OF PENTAGASTRIN FROM GASTROINTESTINAL TRACT IN MAN , 1975, The Lancet.
[45] Kozo Kaibuchi,et al. Role of Rho GTPases in thrombin-induced lung vascular endothelial cells barrier dysfunction. , 2004, Microvascular research.
[46] J. Landry,et al. Regulation of actin dynamics by stress-activated protein kinase 2 (SAPK2)-dependent phosphorylation of heat-shock protein of 27 kDa (Hsp27). , 1999, Biochemical Society symposium.
[47] M. Gaestel,et al. MAPKAP kinase 2 is essential for LPS-induced TNF-alpha biosynthesis. , 1999, Nature cell biology.
[48] P. Guillausseau,et al. Rapid Publication , 1971, Nature.