Soluble forms of E-selectin, ICAM-1 and VCAM-1 are present in the supernatants of cytokine activated cultured endothelial cells

Pigott, Rod; Dillon, L.P.; Hemingway, I.; Gearing, A. J. H.

doi:10.1016/0006-291x(92)91234-h

Cited by 632 publications

(375 citation statements)

References 17 publications

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“…Serum E-selectin must therefore, by implication, be endothelial cellderived, and hence alterations in the serum levels of this adhesion molecule in disease states may reflect changes in the endothelial cell phenotype in vivo. Interestingly, release of E-selectin, ICAM-I, and VCAM-1 from cultured human vascular endothelial cells has been shown to vary in proportion of the degree of surface expression in response to cytokines such as TNFa, which is well established as an important inducer of the expression of these adhesion molecules in vitro (30,31). However, the effect of TNFa on the release of ICAM-1 and VCAM-1 from other cell types (such as fibroblasts) has not been studied.…”

Section: Discussionmentioning

confidence: 99%

Deactivation of vascular endothelium by monoclonal anti–tumor necrosis factor α antibody in rheumatoid arthritis

Paleolog

Hunt

Elliott

et al. 1996

Arthritis & Rheumatism

227

118

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Objective. To assess whether monoclonal antibody to tumor necrosis factor a (TNFa) reduces endothelial activation in rheumatoid arthritis (RA).Methods. Levels of serum E-selectin, intercellular adhesion molecule 1 (ICAM-l), and vascular cell adhesion molecule 1 (VCAM-l), and circulating leukocytes (differential counts) were measured in RA patients before and up to 4 weeks after infusion of either placebo or chimeric anti-TNFa antibody cA2 (1 or 10 mg/kg).Results. Treatment with anti-TNFa decreased serum E-selectin and ICAM-1 levels, with the earliest detectable changes observed on days 1-3 after anti-TNFa infusion. No effect on VCAM-1 levels was detected. In parallel, there was a rapid and sustained increase in circulating lymphocytes. The extent of the decrease in serum E-selectin and ICAM-1 levels and the increase in lymphocyte counts was significantly higher (P I 0.05) in patients in whom a clinical benefit of anti-TNFa was observed (120% response, by Paulus criteria, at week 4) compared with that in patients who failed to respond to anti-TNFa at this time point.Conclusion. We propose that decreased serum levels of adhesion molecules may reflect diminished activation of endothelial cells in the synovial microvas-

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Section: Discussionmentioning

confidence: 99%

Deactivation of vascular endothelium by monoclonal anti–tumor necrosis factor α antibody in rheumatoid arthritis

Paleolog

Hunt

Elliott

et al. 1996

Arthritis & Rheumatism

227

118

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“…Concentrations of circulating E-selectin and VCAM-1 were measured using dual monoclonal antibody two-site ELISAs Pigott et al, 1992). Briefly, microtitre ELISA plates (Nunc Immunoplates, Life Technologies, Paisley, Scotland) were coated overnight with a specific capture antibody (BBIG-E2 for E-selectin, BBIG-V4 for VCAM-1) at a final concentration of 10 tg ml-' in 0.1 M bicarbonate buffer pH 8.9.…”

Section: Sera and Patientsmentioning

confidence: 99%

Circulating intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in human malignancies

Banks

Gearing²,

Hemingway³

et al. 1993

Br J Cancer

288

153

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Summary Cellular adhesion molecules have been implicated in tumour progression and metastasis. This study examines for the first time the serum concentrations of circulating VCAM-1 and E-selectin in a consecutive series of 110 cancer patients seen in a general medical oncology clinic, and confirms and extends previous studies reporting measurement of circulating ICAM-1. Soluble ICAM-1 and VCAM-1 levels were significantly higher in all the patient groups compared with the controls whereas soluble E-selectin was significantly higher in the ovarian, breast and GI cancer groups and lower in the myeloma group. The significance of these results together with the possible sources and stimuli for release of these adhesion molecules are discussed. Sera and patientsBlood samples were obtained from a consecutive series of all patients being seen in a general medical oncology clinic, including those with both localised or advanced disease and those on active therapy or during follow-up. The following malignancies were represented: bladder (n = 6), breast (n = 13), gastrointestinal (n = 18), ovarian (n = 15), renal (n = 12), Hodgkin's disease (n = 15), non-Hodgkin's lymphoma (n = 13), and myeloma (n = 18). Approximately 85% of those with epithelial cancers had clinical evidence of metastases. Samples were allowed to clot, and the serum stored at -70'C until assayed. Samples were also obtained from 89 healthy laboratory and clinical personnel and blood donors (age range 18-60 years) and assayed for E-selectin and VCAM-1. In the case of ICAM-1, a sub-group of 27 of the control samples (age range 24-54 years) were assayed.Assay of soluble adhesion molecules Levels of circulating ICAM-1 were measured with a commercial ELISA kit (British Bio-technology Products, Oxford, UK). Concentrations of circulating E-selectin and VCAM-1 were measured using dual monoclonal antibody two-site ELISAs Pigott et al., 1992). Briefly, microtitre ELISA plates (Nunc Immunoplates, Life Technologies, Paisley, Scotland) were coated overnight with a specific capture antibody (BBIG-E2 for E-selectin, BBIG-V4 for VCAM-1) at a final concentration of 10 tg ml-' in 0.1 M bicarbonate buffer pH 8.9. Standards and samples were added to the plate, incubated for 2 h at room temperature and the bound soluble adhesin of interest was detected by sequential incubation with a specific biotin-labelled antibody (BBIG-E5 for E-selectin, BBIG-V3 for VCAM-1) followed by horseradish peroxidase-conjugated streptavidin (Amersham International, Amersham, UK) and finally tetramethylbenzidine (Universal Biologicals, Kingston-upon-Thames, UK). The reaction was stopped by the addition of 1 M HCI to each well and the O.D. 450 nm measured using a Titertek MS-2 reader (ICN Flow, Rickmansworth, UK). The assays were standardised using a recombinant soluble form of Eselectin or VCAM-1 (Pigott et al., 1991) lacking their transmembrane and cytoplasmic domains and given an arbitrary unitage against which all samples were measured.Statistical analysis Data was analysed using SPSS/PC + . Res...

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“…Release of proinflammatory cytokines at sites of inflammation and immune response causes cell activation and results in augmented cellular ICAM-1 expression [13]. Shedding of ICAM-1 is increased by treatment with TNF-and IL-1 [14]. Circulating sICAM-1 has been reported to be elevated in patients with inflammatory diseases [15][16][17][18][19][20], and excess release of proinflammatory cytokines seems to be related to the elevation of circulating sICAM-1 in these disorders.…”

Section: Introductionmentioning

confidence: 99%

Circulating soluble intercellular adhesion molecule-1 (sICAM-1) in patients with sarcoidosis

Shijubo

Imai

Shigehara³

et al. 1996

Clinical and Experimental Immunology

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sICAM‐1 has been elevated in sera of specific inflammatory diseases, and circulating sICAM‐1 concentrations reflect disease activity in these diseases. We measured circulating sICAM‐1 concentrations and serum angiotensin‐converting enzyme (SACE) activity in patients with sarcoidosis. Patients with sarcoidosis had significantly increased circulating sICAM‐1 concentrations (62.8±33.5U/ml) and SACE activity (23.7±7.4U/l) compared with controls (circulating sICAM‐1 50.9±12.1U/ml, and SACE 13.5±3.8U/l). Successive measurements showed that circulating sICAM‐1 values changed in parallel with disease activity in sarcoidosis. In the progressive disease group (progressed or without change for 2 years or more), circulating sICAM‐1 values (102.2±35.3U/ml) at the time of diagnosis were significantly increased compared with those in the regressive disease group (disappeared or regressed within 2 years) (46.4±12.6U/ml). However, there was no significant difference in SACE activity of the regressive and progressive disease groups. Fifteen patients with a high value of circulating sICAM‐1 (>75U/ml, mean of controls+2s.d.) all had progressive disease, while only 15 of 44 patients with a high value of SACE had progressive disease. Circulating sICAM‐1 will be a useful blood marker to predict outcome and to monitor disease activity in sarcoidosis.

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Soluble forms of E-selectin, ICAM-1 and VCAM-1 are present in the supernatants of cytokine activated cultured endothelial cells

Cited by 632 publications

References 17 publications

Deactivation of vascular endothelium by monoclonal anti–tumor necrosis factor α antibody in rheumatoid arthritis

Deactivation of vascular endothelium by monoclonal anti–tumor necrosis factor α antibody in rheumatoid arthritis

Circulating intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in human malignancies

Circulating soluble intercellular adhesion molecule-1 (sICAM-1) in patients with sarcoidosis

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