Neutrophil-associated, NADPH oxidase-derived superoxide mediates lymphocyte-endethellal cell adhesion in post-ischemic intestinal microvasculature

2001 ◽  
Vol 120 (5) ◽  
pp. A194-A194
Author(s):  
T SHIGEMATSU ◽  
C ROSS ◽  
J MCCORD ◽  
D GRANGER
Keyword(s):  
Cell Adhesion ◽  
Nadph Oxidase

TNF-α-induced endothelial cell adhesion molecule expression is cytochrome P-450 monooxygenase dependent

2003 ◽  
Vol 284 (2) ◽  
pp. C422-C428 ◽  
Author(s):  
Makoto Sasaki ◽  
D. Ostanin ◽  
J. W. Elrod ◽  
T. Oshima ◽  
P. Jordan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Nadph Oxidase ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Tnf Α ◽  
Oxidase Inhibition ◽  
Endothelial Adhesion Molecules ◽  
Cytochrome P 450

It is strongly suspected that cytokine-induced gene expression in inflammation is oxidant mediated; however, the intracellular sources of signaling oxidants remain controversial. In inflammatory bowel disease (IBD) proinflammatory cytokines, such as TNF-α, trigger gene expression of endothelial adhesion molecules including mucosal addressin cell adhesion molecule-1 (MAdCAM-1). MAdCAM-1 plays an essential role in gut inflammation by governing the infiltration of leukocytes into the intestine. Several groups suggest that endothelial-derived reduced NADP (NADPH) oxidase produces signaling oxidants that control the expression of adhesion molecules (E-selectin, ICAM-1, VCAM-1). In addition to NADPH oxidase, cytochrome P-450 (CYP450) monooxygenases have also been shown to trigger cytokine responses. We found that in high endothelial venular cells (SVEC4-10), multiple inhibitors of CYP450 monooxygenases (SKF-525a, ketoconazole, troleandomycin, itraconazole) attenuated TNF-α induction of MAdCAM-1, whereas NADPH oxidase inhibition (PR-39) did not. Conversely, E-selectin, ICAM-1, and VCAM-1 induction requires both NADPH oxidase and CYP450-derived oxidants. We show here that MAdCAM-1 induction may depend exclusively on CYP450-derived oxidants, suggesting that CYP450 blockers might represent a possible novel therapeutic treatment for human IBD.

Neutrophil-associated, NADPH oxidase-derived superoxide mediates lymphocyte-endethellal cell adhesion in post-ischemic intestinal microvasculature

2001 ◽  
Vol 120 (5) ◽  
pp. A194
Author(s):  
Takeharu Shigematsu ◽  
Chris R. Ross ◽  
Joe M. McCord ◽  
D Neil Granger
Keyword(s):  
Cell Adhesion ◽  
Nadph Oxidase

scholarly journals Cell adhesion markedly increases lucigenin-enhanced chemiluminescence of the phagocyte NADPH oxidase

2008 ◽  
Vol 13 (12) ◽  
pp. 1249-1256 ◽  
Author(s):  
Futoshi Kuribayashi ◽  
Satoru Tsuruta ◽  
Tsuyoshi Yamazaki ◽  
Hiroyuki Nunoi ◽  
Shinobu Imajoh-Ohmi ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Nadph Oxidase ◽  
Phagocyte Nadph Oxidase ◽  
Enhanced Chemiluminescence

scholarly journals S17834, a New Inhibitor of Cell Adhesion and Atherosclerosis That Targets NADPH Oxidase

2001 ◽  
Vol 21 (10) ◽  
pp. 1577-1584 ◽  
Author(s):  
Antonio J. Cayatte ◽  
Alain Rupin ◽  
Jennifer Oliver-Krasinski ◽  
Karlene Maitland ◽  
Patricia Sansilvestri-Morel ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Nadph Oxidase

Role of superoxide in hemorrhagic shock-induced P-selectin expression

2000 ◽  
Vol 279 (2) ◽  
pp. H791-H797 ◽  
Author(s):  
Feza M. Akgür ◽  
Mark F. Brown ◽  
Gazi B. Zibari ◽  
John C. McDonald ◽  
Charles J. Epstein ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Nadph Oxidase ◽  
Xanthine Oxidase ◽  
Adhesion Molecule ◽  
Oxygen Radicals ◽  
Whole Body ◽  
Antibody Technique ◽  
Vascular Beds ◽  
Endothelial Cell Adhesion

Superoxide has been implicated in the regulation of endothelial cell adhesion molecule expression and the subsequent initiation of leukocyte-endothelial cell adhesion in different experimental models of inflammation. The objective of this study was to assess the contribution of oxygen radicals to P-selectin expression in a murine model of whole body ischemia-reperfusion, i.e., hemorrhage-resuscitation (H/R), with the use of different strategies that interfere with either the production (allopurinol, CD11/CD18-deficient or p47phox−/− mice) or accumulation [intravenous superoxide dismutase (SOD), mutant mice that overexpress SOD] of oxygen radicals. P-selectin expression was quantified in different regional vascular beds by use of the dual-radiolabeled monoclonal antibody technique. H/R elicited a significant increase in P-selectin expression in all vascular beds. This response was blunted in SOD transgenic mice and in wild-type mice receiving either intravenous SOD or the xanthine oxidase inhibitor allopurinol. Mice genetically deficient in either a subunit of NADPH oxidase or the leukocyte adhesion molecule CD11/CD18 also exhibited a reduced P-selectin expression. These results implicate superoxide, derived from both xanthine oxidase and NADPH oxidase, as mediators of the increased P-selectin expression observed in different regional vascular beds exposed to hemorrhage and retransfusion.

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