Disease relevance of ICAM1

• Human umbilical vein endothelial cell (HUVEC) and bovine aortic endothelial cell (BAEC) induction of ICAM-1 required simultaneous exposure to both hypoxia and hypoglycemia as determined by confocal laser scanning microscopy, ELISA, and Western blot [1].
• Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS [1].
• Inhibition of Rho activity by Clostridium botulinum C3 transferase or by overexpression of RhoA T19N, a dominant-negative mutant of RhoA, decreased LPS-induced ICAM-1 expression [2].
• In situ expression of intercellular adhesion molecule-1 (ICAM-1) mRNA in calves with acute Pasteurella haemolytica pneumonia [3].
• Adenovirus vectors encoding carcinoembryonic antigen (Ad-CEA) or costimulatory molecules CD80, intercellular adhesion molecule-1 (ICAM-1) and leucocyte function-associated antigen-3 (LFA-3) (Ad-STIM) were used to transduce murine bone marrow-derived dendritic cells (BMDC) [4].

High impact information on ICAM1

• Additionally, Rac1 mediates flow-induced stimulation of nuclear factor kappaB (NF-kappaB) and the subsequent expression of intercellular cell adhesion molecule 1 (ICAM-1), an adhesion receptor involved in the recruitment of leukocytes to atherosclerotic plaque [5].
• The distribution of ICAM-1 on bone marrow progenitors, early precursor cells, and accessory cells in conjunction with the function of this molecule in cell-cell interactions suggests that ICAM-1 may play a role in the cell-cell and cell-stromal interactions that regulate hematopoiesis [6].
• ICAM-1 was also detected on bone marrow blasts, proerythroblasts, promyelocytes, and cells of monocyte/macrophage lineage, but was not detected on erythroblasts, normoblasts, neutrophilic myelocytes, metamyelocytes, bands, or on most lymphocytes [6].
• After timed incubation in media with fetal bovine serum, 29% of erythroid burst-forming units (BFU-E), 24% of erythroid colony-forming units (CFU-E), and 52% of granulocyte-macrophage colony-forming units (CFU-GM) bone marrow progenitors expressed ICAM-1 [6].
• Role of the JNK pathway in thrombin-induced ICAM-1 expression in endothelial cells [7].

Biological context of ICAM1

• METHODS: Western blot analysis using anti-ICAM-1 antibody and luciferase assays were performed in cultured endothelial cells after addition of signal transduction inhibitors or transfection of various gene constructs [7].
• Resveratrol was found to inhibit both TNFalpha- and IL-6-induced ICAM-1 gene expression at the promoter, transcriptional and protein levels [8].
• Furthermore, ECs transfected with constitutively active Rac1 (RacV12) showed increases in ICAM-1 promoter activity, intracellular reactive oxygen species (ROS) levels and STAT3 phosphorylation, and these increases were attenuated by resveratrol treatment [8].
• In summary, different stimuli produced similar expression kinetics of VCAM-1 surface protein but different kinetics of ICAM-1 mRNA expression [9].
• Endothelial cell adhesion molecules (AM) intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) are important mediators of cell migration from blood into tissue [9].

Anatomical context of ICAM1

• Northern blot results show that the bovine ICAM-1 gene is expressed in stimulated leukocytes whereas bovine ICAM-3 is expressed predominantly in resting neutrophils [10].
• Modulation of ICAM-1 expression by extracellular glutathione in hyperoxia-exposed human pulmonary artery endothelial cells [11].
• XO increases neutrophil adherence to endothelial cells by a dual ICAM-1 and P-selectin-mediated mechanism [12].
• In lungs of both non-BLAD and BLAD saline-inoculated calves, ICAM-1 expression was present in epithelial cells but occurred in <30% of cells in bronchi, bronchioles, and alveoli [3].
• BSM inhibits the adhesion of lymphocytes when coimmobilized with intercellular adhesion molecule-1 (ICAM-1) and blocks the activation of T lymphocytes when coimmobilized with anti-CD3 [13].

Associations of ICAM1 with chemical compounds

• The predicted number and positions of cysteine residues in bovine ICAM-1 are all conserved among species including bovine ICAM-3 [10].
• These results suggest that extracellular GSH plays a role in regulating hyperoxia-induced ICAM-1 expression in HPAEC and HUVEC [11].
• Negative relationships were also demonstrated between the level of ICAM-1 expression and the total extracellular glutathione concentrations in NAC-treated HPAEC (R = 0.877, P < 0.0005) and HUVEC (R = 0.727, P < 0.0005) [11].
• The ICAM-1 expression was decreased and the GSH concentration was increased with the addition of NAC [11].
• 8-Bromo cyclic AMP, showed no concentration-dependent inhibition of ET-1 release, yet caused a 50% reduction in TNFalpha-stimulated intercellular adhesion molecule-1 (ICAM-1) mRNA levels [14].

Regulatory relationships of ICAM1

• Subthreshold hyperoxia potentiates TNF-alpha-induced ICAM-1 expression on cultured pulmonary microvascular endothelial cells [15].

Other interactions of ICAM1

• Resveratrol suppresses IL-6-induced ICAM-1 gene expression in endothelial cells: effects on the inhibition of STAT3 phosphorylation [8].
• The amount of soluble ICAM-1 that has been released into the culture medium increased after joint exposure to hyperoxia and TNF-alpha [15].
• The kinetics of ICAM-1 mRNA and VCAM-1 protein expression in bovine aortic endothelial cells (BAEC) were determined using quantitative reverse transcriptase polymerase chain reaction (Q-RT-PCR) and flow cytometric analysis, respectively [9].
• These data revealed crocetin could prevent the adhesion of leukocyte to BEC and down-regulation the expression of ICAM-1, and the possible mechanisms might be related to its antioxidant activity, which is through up-regulation of the activity of antioxidant enzymes and protection for mitochondrion [16].

Analytical, diagnostic and therapeutic context of ICAM1

• RESULTS: Treatment of endothelial cells with the JNK-specific inhibitors, SP600125 or JNK inhibitory peptide 1 (JNKI1), resulted in a significant decrease in thrombin-induced ICAM-1 expression as demonstrated by Western blot analysis (67 +/- 3% and 72 +/- 7%, respectively) [7].
• The levels of ICAM-1 expression in the endothelial cells and the concentrations of reduced (GSH) and oxidized glutathione (GSSG) in the media were examined by flow cytometry and spectrophotometry, respectively [11].
• In the presence of 5% fetal bovine serum, lipid A-induced ICAM-1 expression, as measured by radioimmunoassay following 18 h incubation, was enhanced by A78S1 at lower concentrations (.02-.2 micrograms/ mL) but was inhibited at concentrations of 20 micrograms/mL or greater [17].
• The in situ expression of intercellular adhesion molecule-1 (ICAM-1) mRNA in normal and pneumonic lung tissues of Holstein calves with bovine leukocyte adhesion deficiency (BLAD) was compared with that of age-matched non-BLAD Holstein calves by in situ hybridization [3].
• Semiquantitative Realtime RT-PCR showed upregulated transcription of the E- and P-selectin genes in BUVECs within 1h p.i. and of ICAM-1 and VCAM-1 genes within 2h p.i. Maximum transcript levels were observed at 4-6h p.i.; the 24h p.i. gene transcription had declined to control levels [18].

References