Disease relevance of Madcam1

• Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation [1].
• In this study, we examined whether MAdCAM-1 is involved in the pathogenesis of granulomatous colitis induced by peptidoglycan-polysaccharide (PG-PS) [2].
• MAdCAM-1 expression maintained by the presence of bile may regulate T-lymphocyte homing to the lamina propria in obstructive jaundice [3].

High impact information on Madcam1

• The alpha4 integrins, which are constitutively expressed on all human leukocyte subtypes except neutrophils, interact with vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule (MAdCAM-1) on endothelium to mediate selective recruitment of leukocyte subpopulations, other than neutrophils, to sites of inflammation [4].
• Although alpha4 was expressed at lower levels on neutrophils than all other rat leukocytes, this level of expression was sufficient to mediate significant levels of alpha4- and beta1-dependent neutrophil adhesion to rat and human VCAM-1, and alpha4-dependent, but beta1-independent, adhesion to human MAdCAM-1 [4].
• A novel series of pyridazinone-functionalized phenylalanine analogues was prepared and evaluated for inhibition of cellular adhesion mediated by alpha4beta1/VCAM-1 and alpha4beta7/MAdCAM-1 interactions [5].
• HEV express several L-selectin ligands including CD34, GlyCAM-1, MAdCAM-1 and two sulfated glycoproteins (Sgp) of 200 kDa and 170 kDa which remain to be identified [6].
• Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process [1].

Biological context of Madcam1

• Assignment of the Madcam1 gene to rat chromosome 7q11.2-->q12 by fluorescence in situ hybridization, somatic cell hybrids and linkage analysis [7].
• Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups [1].
• CONCLUSIONS: Alteration in MAdCAM-1 expression may be associated with the development of SB graft rejection [8].
• Homology of nucleotide sequences between the mouse and rat MAdCAM-1 ORF was 85.1% with an amino acid identity of 80.5% [9].
• A cDNA clone for rat MAdCAM-1 homologue was isolated from mesenteric lymph nodes by RT-PCR using primers prepared from the exon sequences of the gene isolated from a genomic library of the WKAH rat, using mouse cDNA as a probe [9].

Anatomical context of Madcam1

• The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration [1].
• Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1 [1].
• FTY720 was found to prevent the down-regulation of MAdCAM-1 expression on HEVs in PPs and the up-regulation of its expression on endothelial cells of vessels in the lamina propria while also prolonging small bowel allograft survival [8].
• In the FTY720-treated groups, MAdCAM-1 expression on HEVs in PPs was up-regulated and its expression on endothelial cells of vessels in the lamina propria was down-regulated compared with untreated allograft group [8].
• The area of MAdCAM-1-positive venules and the subsets of infiltrating cells were determined in colonic mucosa by immunohistochemistry [2].

Associations of Madcam1 with chemical compounds

• We performed a semiquantitative analysis of MAdCAM-1 expression during small bowel graft rejection in rat treated with FTY720 [8].
• The present study employs flow cytometry and quantitative immunohistochemistry to assess age-related changes in the numbers of peripheral blood mononuclear cells expressing the homing integrin alpha4beta7 and vascular endothelial cells in the intestine expressing its specific receptor, the address in MAdCAM-1, in inbred Fischer 344 rats [10].

Other interactions of Madcam1

• To distinguish between recognition of MAdCAM-1 and VCAM-1 by alpha 4-containing integrins, recipients were treated with mAb 5F10 against rat VCAM-1 [11].
• L-selectin (CD62L), the ligand for MAdCAM-1, was strongly expressed on CD45RChighOX62+ cells but not on CD45RClowOX62+ cells [12].

Analytical, diagnostic and therapeutic context of Madcam1

• CONCLUSIONS: Changes in the number of T lymphocytes and MAdCAM-1 expression are associated with the presence of bile in the gastrointestinal tract and are inversely correlated with the frequency of bacterial translocation induced by CBD ligation [3].

References