Soluble Vascular Cellular Adhesion Molecule-1 Research Articles

Soluble adhesion molecules: marker of pre-eclampsia and intrauterine growth restriction

Objective: This study monitored circulating plasma levels of soluble vascular cellular adhesion molecule-1 (sVCAM-1), intracellular adhesion molecule-1 (sICAM-1) and soluble E-selectin (sE-selectin)in women with healthy pregnancies, with pregnancy-induced hypertension (PIH), with pre-eclampsia and with pregnancies with isolated intrauterine growth restriction (IUGR) in order to determine whether elevatedconcentrations have a predictive value for the clinical signs of those pregnancy-induced disorders.Methods: Plasma concentrations of sVCAM-1, sICAM-1 and sE-selectin were determined in healthypregnant women at each trimester of pregnancy and in pregnant women with PIH, pre-eclampsia and IUGR using commercial kits.Results: In the group of healthy pregnant women, plasma levels of sVCAM-1,sICAM-1 and sE-selectin did not change throughout pregnancy. No significant differences in the levels of these molecules were observed between healthy pregnant women at the third trimester of pregnancyand women with PIH. In addition, concentrations of soluble adhesion molecules were significantly higher in women with pre-eclampsia than in the group of women with healthy pregnancies. Only sVCAM-1 andsE-selectin levels were significantly higher in women with IUGR compared to healthy pregnant women.Conclusions: Abnormally circulating levels of sVCAM-1, sICAM-1 and sE-selectin may have a predictivevalue for pre-eclampsia and IUGR, as they may be linked with endothelial activation and/or damage.

Increased plasma levels of soluble vascular cellular adhesion molecule-1 in patients with chest pain and angiographically normal coronary arteries

Aims: To assess plasma levels of vascular cellular adhesion molecule-1, a marker of endothelial dysfunction, in patients presenting with coronary syndromes submitted to coronary angiography. Methods and results: Plasma levels of soluble vascular cellular adhesion molecule-1 were measured by enzymatic immunoabsorbent assay in eight patients with angina-like chest pain and angiographically normal coronary arteries; in 14 patients with stable angina and in 18 patients with unstable angina, both with coronary lesions by angiography, and in 10 healthy volunteers. Levels of soluble vascular cellular adhesion molecule-1 were higher in unstable angina patients (1777±161 SE pg ml −1) compared to patients with stable angina (1178±206 SE pg ml −1, P<0.05). Moreover, patients with angina-like chest pain and normal coronary arteries had significantly higher soluble vascular cellular adhesion molecule-1 levels (2307±295 SE pg ml −1) compared to stable angina patients ( P<0.05), but similar levels compared to unstable angina patients. Patient groups had higher values of soluble vascular cellular adhesion molecule-1 compared to the control group (734±97 SE pg ml −1). Conclusions: Increased levels of soluble vascular cellular adhesion molecule-1 are associated with coronary artery disease in patients with anatomically established lesions. In patients free of flow-limiting lesions and angina-like chest pain, high levels of this marker may indicate endothelial dysfunction.

Soluble cellular adhesion molecules in proliferative vitreoretinopathy and proliferative diabetic retinopathy

PURPOSE. To measure vitreous levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cellular adhesion molecule-1 (sVCAM-1) in the eyes of patients with retinal detachment (RD) due to proliferative diabetic retinopathy (PDR) or proliferative vitreoretinopathy (PVR) and to determine whether the levels of these mediators correlated with clinical parameters of disease. METHODS. Undiluted vitreous specimens were collected from 50 eyes of 48 patients undergoing vitrectomy for traction RD due to PDR (21 specimens) and recurrent RD due to PVR (19 specimens). Control vitreous specimens were obtained from patients undergoing macular hole repair (10 specimens). The levels of sICAM-1 and sVCAM-1 were measured in each sample by specific enzyme-linked immunoadsorbent assays. RESULTS. Vitreous levels of sICAM-1 were significantly increased in vitreous specimens from both PVR (median ± SD; 12.0 ± 76.3 ng/ml; P < 0.01) and PDR (8.4 ± 24.0 ng/ml; P < 0.01) when compared to vitreous from eyes with macular holes (0.3 ± 4.2 ng/ml). Vitreous levels of sVCAM-1 were significantly increased in both PVR (36.5 ± 255.2 ng/ml; P < 0.001) and PDR (26.2 ± 93.5 ng/ml; P < 0.01) when compared to control vitreous (17.7 ± 7.8 ng/ml). The vitreous levels of sICAM-1 were higher in cases of PDR which developed recurrent proliferative disease (P < 0.01) and recurrent RD (P = 0.01), whereas the levels of sICAM-1 in PVR and sVCAM-1 in PDR and PVR did not significantly correlate with these clinical parameters. CONCLUSIONS. Soluble forms of ICAM-1 and VCAM-1 are increased in the vitreous cavity of patients with RD due to PDR or PVR, reflecting the inflammatory nature of these conditions and suggesting a possible role for these mediators in the pathogenesis of proliferative retinal disease. The vitreous levels of these sCAMs at the time of surgery may serve as a marker of inflammation, but their specific levels do not predict the likelihood of recurrent proliferation or surgical anatomic success in most cases of PVR and PDR.

Increased mucosal concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), sE-selectin, and interleukin-8 in active ulcerative colitis.

Cell surface adhesion molecules (CAM) are important promotors of the immunoinflammatory cascade. The circulating levels of soluble intercellular adhesion molecule 1 (ICAM-1) have previously been shown to correlate with disease activity in inflammatory bowel disease. The primary aim of this study was consequently to investigate if this also applies to mucosal levels of soluble ICAM-1. We measured soluble ICAM-1 levels in intestinal biopsy specimens and the endoscopic activity of 69 patients with ulcerative colitis (UC) and 14 controls and found that the median concentration of soluble ICAM-1 was significantly higher in patients with moderately or very active UC (15.0 ng/ml) as compared to slightly active (9.8 ng/ml) and inactive UC (9.5 ng/ml) as well as controls (6.5 ng/ml) (P < 0.005). To further elucidate the interactions, two other CAM [E-selectin and vascular cellular adhesion molecule 1 (VCAM-1)], together with interleukin-8 (IL-8), IL-2 receptor (IL-2R) alpha and beta chains, were also measured. A significant trend towards higher soluble E-selectin levels in biopsies with active UC (1.8 pg/ml) as compared to inactive UC (1.3 pg/ml) and to controls (< 1.0 pg/ml) (P < 0.01) was also found. In contrast, soluble VCAM-1 was barely detectable in biopsies from two UC patients. A significant correlation was found between soluble ICAM-1 and IL-8 concentrations (r = 0.46; P < 0.0001), and between sICAM-1 and sIL-2R alpha concentrations (r = 0.69; P < 0.0001), while sIL-2R beta was not detected. This study shows that intestinal ICAM-1 and E-selectin correlate with endoscopic activity of UC and with IL-8 and IL-2R alpha levels. These mediators may be useful in monitoring mucosal inflammation in studies exploring the therapeutical potential of targeting CAM. The lack of detectable VCAM-1, which is induced only in venous endothelium is interesting. It may suggest that intestinal inflammation mainly affects arterial endothelial cells and support the theory that intestinal vasculitis is involved in the pathogenesis of inflammatory bowel disease.

Quantitative detection of soluble adhesion molecules in sera of melanoma patients correlates with clinical stage.

Adhesion is crucial in the metastatic process of malignant tumours. Recently, the expression of certain selectins on intratumoral vessels has been shown to be associated with the clinical outcome of melanoma patients. For the first time, this study examines the serum concentrations of circulating soluble vascular cellular adhesion molecule 1 (CD 106), endothelial leucocyte adhesion molecule (CD62E), sP-selectin (CD62P) and sCD44v5 in comparison to soluble intercellular adhesion molecule 1 (sICAM-1, CD54) in a series of 34 melanoma patients at different clinical stages and 11 normal donors using ELISA: sICAM-1 and sP-selectin levels were statistically elevated in all subgroups of melanoma patients compared to controls (p < 0.01). Circulating ICAM-1 as well as sP-selectin might be valuable additional serological tumour markers which correspond to tumour load and correlate with progression of malignant melanoma. Measurement of sICAM-1 and sP-selectin serum levels might therefore provide a sensitive tool for monitoring the clinical course of melanoma.

Serum levels of soluble vascular cellular adhesion molecule-1(sVCAM-1) during treatment with interferon alpha(INFα) in chronic hepatitis C: [formula omitted]: 3rd Department of Internal Medicine, Wakayama Medical University, Japan

Objective. Because recruitment and retention of lymphoid cells appear to be critical components of the pathogenesis of lichen planus, we have compared the expression and distribution of a panel of vascular adhesion molecules (ELAM-1, P-selectin, 1CAM-1, VCAM-1, PECAM-1, CD34) and leukocyte adhesion molecule ligands (LFA-1, Mac-1, VLA4, L-selectin) in biopsies of this disease.Study design. Frozen sections of 12 clinically and histologically confirmed cases of lichen planus and 9 normal control tissues were evaluated immunohistochemically with a standard 1-day avidin-biotin peroxidase technique. Staining intensity of vascular endothelium was evaluated semiquentitatively. Three microvascular zones or compartments were defined and evaluated separately.Results. Generally, different staining patterns were observed in association with the various endothelium-associated adhesion molecules. In normal controls, PECAM was intensely expressed, and VCAM-1 was weakly expressed. Intermediate staining was associated with ELAM-1, P-selectin, ICAM-1, and CD34. Staining within the three microvascular compartments frequently showed variations in intensity. In lichen planus, increased staining for ELAM-1, P-selectin, ICAM-1, and VCAM-1 was evident in one or more of the microvascular compartments. In the subepithelial vascular compartment where the infiltrate was the most dense, VCAM-1 appeared to show the greatest positive change. Almost all cells in the lichen planus infiltrates stained positive for 1CAM-1, L-selectin, LFA-1, and VLA4, and large numbers of cells also exhibited VCAM-1, PECAM-1, and Mac-1 immunoreactivity.Conclusions. It appears that upregulation of ELAM-1, ICAM-1, and VCAM-1 (especially by endothelial cells in the subepithelial vascular plexus) could play a role in the pathogenesis of lichen planus. The expression of leukocyte receptors L-selectin, LFA-1, and VLA4 by most of the cells in the lichen planus infiltrate suggest that these molecules may be responsible for recruitment as well as retention in the active lichen planus lesion.