scholarly journals Involvement of oxidative stress and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in inflammatory bowel disease

2011 ◽  
Vol 48 (2) ◽  
pp. 112-116 ◽  
Author(s):  
Satoshi Tanida ◽  
Tsutomu Mizoshita ◽  
Takashi Mizushima ◽  
Makoto Sasaki ◽  
Takaya Shimura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Bowel Disease ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Bowel Disease ◽  
Cell Adhesion Molecule ◽  
Inflammatory Bowel ◽  
Cell Adhesion Molecule 1

scholarly journals Is the New Approach in Inflammatory Bowel Disease Treat-to-Target?

2021 ◽  
Vol 12 (1) ◽  
pp. 1-14
Author(s):  
Vinod Kumar P ◽  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Cell Adhesion ◽  
Crohn's Disease ◽  
Adhesion Molecule ◽  
Bowel Disease ◽  
Cell Adhesion Molecule ◽  
Inflammatory Bowel ◽  
Cell Adhesion Molecule 1 ◽  
Chronic Intestinal Inflammation

Inflammatory bowel disease is a chronic inflammatory disease of which the etiology is unknown. Ulcerative colitis and Crohn's disease are the two main entities of inflammatory bowel disease that are challenging clinicians. In addition to tumor necrosis factor blockers, this overview summarizes current and future new drugs, in the treatment of inflammatory bowel disease according to their goals. The infiltration of lymphocytes into the intestinal lining is a target for therapeutic purposes in inflammatory bowel disease. The vascular cell adhesion molecule-1 and the mucosal addressin cell adhesion molecule-1 are a family of integrins for the alpha4 that are specifically expressed in the alimentary canal on vascular endothelial cells. In Crohn's disease, the alpha4beta7 integrin, and its endothelial receptor, the mucosal addressin cell adhesion molecule-1, have proven to be a relevant factor in the development of chronic intestinal inflammation. New biological and chemical drugs are emerging, with additional molecules pending approval.

scholarly journals Increased expression of cell adhesion molecule P-selectin in active inflammatory bowel disease.

Gut ◽  
1995 ◽  
Vol 36 (3) ◽  
pp. 411-418 ◽  
Author(s):  
G M Schurmann ◽  
A E Bishop ◽  
P Facer ◽  
M Vecchio ◽  
J C Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Bowel Disease ◽  
Cell Adhesion Molecule ◽  
Active Inflammatory Bowel Disease ◽  
Inflammatory Bowel

CCL25 and CCL28 promote α4β7-integrin-dependent adhesion of lymphocytes to MAdCAM-1 under shear flow

2008 ◽  
Vol 294 (5) ◽  
pp. G1257-G1267 ◽  
Author(s):  
Alice Miles ◽  
Evaggelia Liaskou ◽  
Bertus Eksteen ◽  
Patricia F. Lalor ◽  
David H. Adams
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Human Lymphocytes ◽  
Adhesion Assay ◽  
Lymphocyte Adhesion ◽  
Chemokine Ligand ◽  
Inflammatory Bowel ◽  
Cell Adhesion Molecule 1

Inflammatory bowel disease is characterized by the recruitment of lymphocytes to the gut via mucosal vessels. Chemokines are believed to trigger α4β1- and α4β7-integrin-mediated adhesion to vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) on mucosal vessels, although the contribution of each pathway and the chemokines involved are not well characterized. These interactions occur under conditions of hemodynamic shear, which is critical in determining how lymphocytes integrate chemokine signals to promote transmigration. To define the role of specific chemokines in mediating lymphocyte adhesion to VCAM-1 and MAdCAM-1, we studied the ability of immobilized chemokines to activate adhesion of human lymphocytes in a flow-based adhesion assay. Adhesion to immobilized MAdCAM-1 was α4β7 dependent, with no contribution from α4β1, whereas α4β1 mediated rolling and static adhesion on VCAM-1. Immobilized CC-chemokine ligand (CCL) 25 and CCL28 were both able to trigger α4β7-dependent lymphocyte arrest on MAdCAM-1 under shear, highlighting a potential role for these chemokines in the arrest of lymphocytes on postcapillary venules in the gut. Neither had any effect on adhesion to VCAM-1, suggesting that they selectively trigger α4β7-mediated adhesion. Immobilized CCL21, CCL25, CCL28, and CXC-chemokine ligand (CXCL) 12 all converted rolling adhesion to static arrest on MAdCAM-1 by activating lymphocyte integrins, but only CCL21 and CXCL12 also triggered a motile phenotype characterized by lamelipodia and uropod formation. Thus α4β1/VCAM-1 and α4β7/MAdCAM-1 operate independently to support lymphocyte adhesion from flow, and chemokines may act in concert with one chemokine triggering integrin-mediated arrest and a second chemokine promoting motility and transendothelial migration.

scholarly journals Anti-Atherogenic Effects of Orlistat on Obesity-Induced Vascular Oxidative Stress Rat Model

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 251
Author(s):  
Zaidatul Akmal Othman ◽  
Zaida Zakaria ◽  
Joseph Bagi Suleiman ◽  
Wan Syaheedah Wan Ghazali ◽  
Mahaneem Mohamed
Keyword(s):  
Oxidative Stress ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Inflammatory Marker ◽  
Density Lipoprotein ◽  
Normal Group ◽  
Anti Inflammatory ◽  
Cell Adhesion Molecule 1 ◽  
Vascular Oxidative Stress

Obesity is typically linked to oxidative stress and inflammation, which lead to vascular damage and initiate the progression of atherosclerosis. The aim of this study was to determine the anti-atherosclerotic effect of orlistat on obesity-induced vascular oxidative stress in obese male rats. Twenty-four male Sprague–Dawley rats were categorized into two groups: normal (Normal group, n = 6) and high-fat diet (HFD group, n = 12). After six weeks, obese rats in the HFD group were administered either with distilled water (OB group) or orlistat 10 mg/kg/day (OB/OR group) for another six weeks. The OB group had a significant increase in lipid profiles (total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL)) and decrease in high-density lipoprotein (HDL) level compared to the Normal group. The aortic antioxidants enzymes activities (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), and catalase (CAT)) as well as total glutathione (GSH) and total antioxidant capacity (TAC) of the OB group were significantly decreased compared to the Normal group. Furthermore, pro-inflammatory atherosclerotic markers (tumour necrosis factor-alpha (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), and intercellular cell adhesion molecule-1 (ICAM-1)) expressions were increased significantly, and anti-inflammatory marker (interleukin-10 (IL-10)) was decreased significantly in the OB group compared to the Normal group. Treatment with orlistat significantly improved lipid profile, increased antioxidant enzymes and expression of anti-inflammatory markers, and decreased the expression of the pro-inflammatory marker compared to the OB group. These findings may suggest the therapeutic effect of orlistat in attenuating the progression of the atherosclerotic stage in obesity.

scholarly journals The Presence of Cholesteryl Ester Transfer Protein (CETP) in Endothelial Cells Generates Vascular Oxidative Stress and Endothelial Dysfunction

Biomolecules ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 69
Author(s):  
Amarylis C. B. A. Wanschel ◽  
Daniele M. Guizoni ◽  
Estela Lorza-Gil ◽  
Alessandro G. Salerno ◽  
Adriene A. Paiva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Dysfunction ◽  
Transgenic Mice ◽  
Cholesteryl Ester Transfer Protein ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Transfer Protein ◽  
Cell Adhesion Molecule 1

Endothelial dysfunction precedes atherosclerosis and is an independent predictor of cardiovascular events. Cholesterol levels and oxidative stress are key contributors to endothelial damage, whereas high levels of plasma high-density lipoproteins (HDL) could prevent it. Cholesteryl ester transfer protein (CETP) is one of the most potent endogenous negative regulators of HDL-cholesterol. However, whether and to what degree CETP expression impacts endothelial function, and the molecular mechanisms underlying the vascular effects of CETP on endothelial cells, have not been addressed. Acetylcholine-induced endothelium-dependent relaxation of aortic rings was impaired in human CETP-expressing transgenic mice, compared to their non-transgenic littermates. However, endothelial nitric oxide synthase (eNOS) activation was enhanced. The generation of superoxide and hydrogen peroxide was increased in aortas from CETP transgenic mice, while silencing CETP in cultured human aortic endothelial cells effectively decreased oxidative stress promoted by all major sources of ROS: mitochondria and NOX2. The endoplasmic reticulum stress markers, known as GADD153, PERK, and ARF6, and unfolded protein response effectors, were also diminished. Silencing CETP reduced endothelial tumor necrosis factor (TNF) α levels, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression, diminishing monocyte adhesion. These results support the notion that CETP expression negatively impacts endothelial cell function, revealing a new mechanism that might contribute to atherosclerosis.

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