Disease relevance of ICAM-1

• This study investigated the expression of intercellular adhesion molecule-1 (ICAM-1; CD54) by cells of the central nervous system (CNS) during acute experimental allergic encephalomyelitis (EAE) and chronic relapsing EAE (CREAE) [1].
• Eosinophils play an important role in the development of bronchial asthma, and the association between ICAM-1 and activation and migration of local eosinophils is attracting attention [2].
• In pulmonary genetic diseases, such as emphysema and cystic fibrosis, proteases can also favour the development of local immunodeficiency by degrading key regulators of the immune response, such as CD4, CD8, IgG, ICAM-1 and C3b receptors [3].
• Regulation of ICAM-1 and IL-6 in myocardial ischemia: effect of reperfusion [4].
• Continuous ICAM-1 expression might be related to stenosis of the eustachian tube [5].

High impact information on ICAM-1

• Furthermore, Ox-LDL stimulated the expression of intercellular adhesion molecule-1 (ICAM-1) in the porcine coronary arterial endothelium [6].
• Treatment of the arteries with phorbol 12-myristate 13-acetate, a potent stimulator of PKC, induced ICAM-1 expression and enhanced the endothelial adhesiveness to PMNs and PMN-induced EDR impairment, mimicking the effects of Ox-LDL [6].
• Anti-intercellular adhesion molecule-1 (ICAM-1), anti-vascular cell adhesion molecule-1 (VCAM-1), anti-fibrin, anti-fibrinogen, and anti-tissue factor (TF) conjugated ELIPs were used, and immunohistochemistry (IHC) confirmed the presence or absence of molecular expression [7].
• The Leumedin NPC 15669 (a drug that inhibits leukocyte recruitment) and an antibody to intercellular adhesion molecule-1 (ICAM-1) both prevented neutrophil recruitment and goblet cell degranulation, implicating leukocytes in the response [8].
• Cloning of porcine intercellular adhesion molecule-1 and characterization of its induction on endothelial cells by cytokines [9].

Chemical compound and disease context of ICAM-1

• Amifostine protected the middle ear from radiation injury, and we found that the expression of ICAM-1 in the middle ear mucosa was down-regulated [5].

Biological context of ICAM-1

• These findings suggest that the induction of ICAM-1 on CNS endothelia may be important in antigen presentation or in promoting lymphocyte extravasation across the blood-brain barrier in inflammatory disorders of the CNS [1].
• These results suggest that TGF-beta 1 causes neutrophil-mediated lung injury, possibly through upregulation of ICAM-1 on endothelial cells, and might be important in the pathogenesis of lung injury [10].
• Chondrocyte-peripheral blood mononuclear cell interactions: the role of ICAM-1 [11].
• Gene expression in a swine model of right ventricular hypertrophy: intercellular adhesion molecule, vascular endothelial growth factor and plasminogen activators are upregulated during pressure overload [12].
• Adhesion of monocytes to xenogeneic tissue with or without endothelium and the endothelial cell expression of E-selectin, intercellular adhesion molecule 1, vascular adhesion molecule 1, and major histocompatibility complex class II antigens were investigated 1, 3, and 7 days after seeding [13].

Anatomical context of ICAM-1

• In the CNS of normal guinea pigs, only a few endothelial cells expressed detectable levels of ICAM-1, whereas during the active phases of the disease ICAM-1 was present on cells of the perivascular infiltrate and the endothelia of both lesion- and non-lesion-associated blood vessels [1].
• These results suggest that lysoPC in Ox-LDL induces endothelial ICAM-1 expression, which facilitates PMN adherence to endothelium and the subsequent augmentation of PMN-induced EDR impairment [6].
• Correlation between ICAM-1 and functional recovery of piglet myocardium with leukocyte-depleted reperfusion [14].
• In addition, HDE exposure of epithelial cells results in an approximate twofold increase in ICAM-1 expression as determined by flow cytometry analysis [15].
• The expression of intercellular adhesion molecule-1 (ICAM-1) by chondrocytes under inflammatory conditions has been well documented [11].

Associations of ICAM-1 with chemical compounds

• Coincubation with staurosporine or calphostin C, inhibitors of PKC, during treatment of the arteries with Ox-LDL or lysoPC attenuated the augmentative effects of Ox-LDL and lysoPC on endothelial ICAM-1 expression, endothelial adhesiveness to PMNs, and PMN-induced EDR impairment [6].
• Solution hybridization demonstrated a 2.5-fold increase in steady-state levels of ICAM-1 mRNA in cells exposed to chrysotile asbestos for 8 hr [16].
• Indoxyl sulfate administration was observed to enhance the mRNA levels of ICAM-1 as well as those of TGF-beta 1, TIMP-1 and pro alpha 1 (I) collagen in the renal cortex of 5/6-nephrectomized uremic rats [17].
• The relationship between the protective effect of amifostine and decreased intercellular adhesion molecule 1 expression [5].
• Western blot analysis indicated that PAF upregulated the expression of intercellular adhesion molecule-1 in cultured coronary microvascular endothelial cells [18].

Other interactions of ICAM-1

• In the absence of cytokine stimulation, chondrocyte-peripheral blood mononuclear cell (PBMC) interactions were unaffected by inhibition of ICAM-1-dependent pathways but were significantly reduced by blockade of CD18- and RGD-dependent pathways [11].
• Additionally, the mRNA expression for IL-6R, ICAM-1, MCP-1, and TGF-beta was determined in each organ [19].
• After laser-assisted microdissection of different lung cell types, mRNA expression of IL-8 and ICAM-1 was determined using TaqMan real-time PCR normalized to hypoxanthine phosphoribosyltransferase (HPRT) [20].
• TGF-beta 1 causes increased endothelial ICAM-1 expression and lung injury [10].
• In co-cultivation with the brain endothelial cell model, the malaria-activated PBMC stimulated the expression of E-selectin and ICAM-1 on the PBCEC [21].

Analytical, diagnostic and therapeutic context of ICAM-1

• These results suggest that adhesion molecule like ICAM-1 plays a major role in deteriorating myocardial function during the reperfusion, possibly by leukocyte-mediated inflammatory process [14].
• At 1, 3, 6, 9 and 12 weeks of culture, mRNA was obtained from porcine PE-cells so that the expression of SLA class II and ICAM-1 genes could be examined by reverse transcriptase-polymerase chain reaction [22].
• TGF-beta 1 (1 ng/ml) increased ICAM-1 and ICAM-1 mRNA expression in HUVEC, as assessed by flow cytometry and Northern blot analysis, respectively [10].
• RESULTS: Coculture of human Mo with pig aortic EC (PAEC) resulted in 1.7-fold and 2-fold higher induction of Mo TF and Mo intercellular adhesion molecule-1, respectively, when compared with coculture with human aortic endothelial cells (HAEC) [23].

References