Disease relevance of SELE

• Expression of endothelial-leukocyte adhesion molecule-1 in elicited late phase allergic reactions [1].
• In addition, GMP140 was found to bind to the cell surface of a number of cell lines derived from various carcinomas but not from melanomas, whereas ELAM-1 bound only colon carcinoma cell lines [2].
• Endothelial leukocyte adhesion molecule-1 expression by endothelial venules was detected in 17 of 20 cases of Hodgkin's disease, in 2 of 4 cases of T-NHL, and in 5 of 5 cases of diffuse lymphadenitis [3].
• Cytokine-containing cells and ELAM-1-positive high endothelial venules (HEV) were extremely rare in lymph nodes involved by follicular lymphadenitis (12 cases) or B-NHL (16 cases) [3].
• ELAM-1 reacted with endothelial cells lining venules and capillaries in chronic progressive sarcoidosis and in the active phase of UIP but not in the stationary phases of both diseases [4].

Psychiatry related information on SELE

• Serum levels of soluble intercellular adhesion molecule-1 and soluble endothelial leukocyte adhesion molecule-1 in Alzheimer's disease [5].

High impact information on SELE

• The neutrophil selectin LECAM-1 presents carbohydrate ligands to the vascular selectins ELAM-1 and GMP-140 [6].
• Furthermore, ELFT is expressed specifically in cell types that bind to ELAM-1, suggesting that this enzyme is an important regulator of inflammatory events in vivo [7].
• ELAM-1, a LECCAM found on the surface of activated endothelial cells, can mediate adhesion of neutrophils, monocytes, and certain cell lines to endothelial cells in vitro [7].
• We propose that specific alpha(1,3)fucosyltransferases regulate cell adhesion to ELAM-1 by modulating cell surface expression of one or more alpha(2,3)sialylated, alpha(1,3)fucosylated lactosaminoglycans represented by the sialyl Lewis x carbohydrate determinant [8].
• Adhesion of circulating leukocytes to the vascular endothelium during inflammation is mediated in part by their interaction with the endothelial-leukocyte adhesion molecule ELAM-1 [8].

Chemical compound and disease context of SELE

• For example, some adenocarcinoma cell lines express the complex carbohydrate (sialyl Lewis x) recently shown to be a ligand for ELAM-1 [9].
• ELAM selectin expression in breast carcinomas detected by automated and quantitative immunohistochemical assays [10].
• High-level endothelial E-selectin (CD62E) cell adhesion molecule expression by a lipopolysaccharide-deficient strain of Neisseria meningitidis despite poor activation of NF-kappaB transcription factor [11].
• Objectives To determine if 6 weeks of therapy with levocetirizine 5 mg once daily would also induce any decrease in serum levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial leucocyte adhesion molecule-1 (ELAM-1) or P-selectin in subjects with CU and chronic autoimmune urticaria [12].
• Before steroid treatment, patients with atopic dermatitis demonstrated significantly higher serum levels of sIL-2R, ICAM-1, and ECP than healthy controls (P < 0.001), whereas ELAM-1 levels were not different between the groups [13].

Biological context of SELE

• Our results suggest an age-specific effect of the SELE L/F554 polymorphism on blood pressure levels [14].
• Measurements of blood pressure 11 years before (t(-11)) and at the time of recruitment (t(0)), and all other measurements necessary for the analysis (body mass index, lipids, SELE genotypes) were available [14].
• The location of SELE on chicken Chr 8 was independently established by linkage analysis of COM0185, an (AT)16 microsatellite locus identified in a BAC clone that contained SELE [15].
• The association between the IL-1 system and atherosclerosis is complex and may vary as a result of a number of factors, such as stage of disease, clinical phenotype, and possibly population characteristics.The E-selectin gene (SELE) Arg128, 98T, and Phe554 alleles may increase the risk of atherosclerosis, but not necessarily the risk of MI [16].
• Methods: Primary cultures of HVEC were examined for expression of the adhesion molecules ICAM1, VCAM1 and E-selectin (SELE) after non viral siRNA transfection [17].

Anatomical context of SELE

• Three differentially expressed selectin genes (SELE, SELP, and SELL), important in the initial stages of leukocyte extravasation, have been reported in mammals [15].
• Expression of ELAM-1 transcripts in cultured human endothelial cells is induced by cytokines, reaching a maximum at 2 to 4 hours and decaying by 24 hours; cell surface expression of ELAM-1 protein parallels that of the mRNA [18].
• A full-length complementary DNA (cDNA) for ELAM-1 has now been isolated by transient expression in COS cells [18].
• In contrast the activation-independent adhesion of CD4+ T cell to ELAM-1 molecules does not lead to T cell stimulation as measured by proliferation, IL-2R alpha expression, or cytokine release [19].
• These data document distinct roles for ICAM-1, ELAM-1, and VCAM-1 during basophil, eosinophil, and neutrophil adhesion in vitro, and suggest a novel mechanism for the recruitment of eosinophils and basophils to sites of inflammation in vivo [20].

Associations of SELE with chemical compounds

• Endothelial leukocyte adhesion molecule-1 (ELAM-1), a cell surface glycoprotein expressed by cytokine-activated endothelium, mediates the adhesion of blood neutrophils [18].
• In 7 of 7 atopic patients but in only 1 of 4 apparently normal controls, allergen induced appearance of ELAM-1 on EC [1].
• Leukocyte adherence to endothelium is in part mediated by the transient expression of endothelial-leukocyte adhesion molecule 1 (ELAM-1) on endothelial surfaces stimulated by tumor necrosis factor alpha (TNF), interleukin (IL) 1, or bacterial lipopolysaccharide (LPS) [21].
• In nuclear runoff experiments with cultured human umbilical vein endothelial cells (HUVEC), we demonstrate that transcriptional activation of the ELAM-1 gene occurs following stimulation with TNF [21].
• Treatment of resting endothelial cells with three different protein synthesis inhibitors, cycloheximide (CHX), anisomycin, and emetine, caused an increase in the steady-state level of ELAM-1 mRNA above that observed with IL (interleukin)-1 alone [22].

Physical interactions of SELE

• The NF kappa B binding sequence was found to be necessary and sufficient for superinduction of the ELAM-1 gene by CHX [22].
• We have examined the contributions of endothelial-leukocyte adhesion molecule-1 (ELAM-1) and the complex of leukocyte surface adhesion molecules designated CD11/CD18 to the adhesion of human polymorphonuclear leukocytes (PMN) to cultured human endothelial cells (HEC), activated by rIL-1 beta for 4 or 24 h [23].
• Here we show that a third pathway involving the rapidly inducible endothelial cell-surface adhesion molecule ELAM-1 contributes to the binding of resting CD4+ T cells to IL-1-induced human endothelial cells [24].
• TNF induced increased binding of anti-endothelial leukocyte adhesion molecule (ELAM)-1 mAb by 2 hours that was associated with polymorphonuclear leukocyte accumulation, and increased binding of anti-intercellular adhesion molecule (ICAM)-1 mAb by 9 hours that was associated with the onset of progressive mononuclear leukocyte accumulation [25].

Regulatory relationships of SELE

• PKC blockade with H7 does not inhibit activation of these NF-kappa B-like proteins but does inhibit ELAM-1 gene transcription [21].
• Surprisingly, higher concentrations of verapamil (> 12.5 micrograms/ml) or Ro 40-5967 (5 micrograms/ml) significantly enhanced IL-1-induced expression of ELAM-1 [26].
• ELAM-1 was expressed on endothelium in the inactive-chronic lesions from three of five HAM/HAM/TSP, but was not detectable in the spinal cords of controls [27].
• With IL-1 beta activation of these cells, ELAM-1 was expressed strongly and the expression of ICAM-1 was enhanced [28].
• TNF-alpha and IL-10 enhanced ELAM-1 on DU 145, but EosA 24 hr supematants failed to do so [29].

Other interactions of SELE

• Eosinophils bound specifically to both recombinant soluble ELAM-1 and recombinant soluble VCAM-1 [30].
• Sequence analysis of the 5' flanking region of the ELAM-1 gene reveals consensus DNA-binding sequences for two known transcription factors, NF-kappa B and AP-1 [21].
• Furthermore, ELAM-1 mRNA was found in the presence of all three protein synthesis inhibitors without IL-1 treatment [22].
• We measured as endothelial activation parameters the expression of endothelium-leukocyte adhesion receptor-1 (ELAM-1, E-selectin), major histocompatibility complex (MHC) class II antigens, interleukin 1 (IL-1), interleukin 6 (IL-6), and prostacyclin [31].
• The endothelial leukocyte adhesion molecule (ELAM-1) was not expressed on chondrocytes and was not induced by IL1-alpha [32].

Analytical, diagnostic and therapeutic context of SELE

• ELAM-1 expression occurred concurrently with the development of inflammatory cell infiltrates by 3-4 h after intradermal injection [1].
• Soluble adhesion molecules increased in the untreated control group (endothelial leukocyte adhesion molecule from 92 +/- 14 to 192 +/- 29 ng/mL; intercellular adhesion molecule-1 from 480 +/- 110 to 850 +/- 119 ng/ mL) and returned almost to normal values in the enalaprilat patients [33].
• Northern blot studies revealed by far the highest expression of the murine ELAM-1 gene in heart tissue and only low expression in lung tissue of IL-1-treated mice [34].
• Flow cytometry was utilized to assess the expression of ELAM-1 and ICAM-1, expressed as percent shift from baseline expression [35].
• The distribution and localization of ICAM-1, VCAM-1, and ELAM-1 was determined in the pancreatic specimens by immunohistochemistry [36].

References