Cytokine-induced cell surface expression of adhesion molecules in vascular endothelial cellsIn vitro

2001 ◽  
Vol 21 (1) ◽  
pp. 68-71 ◽  
Author(s):  
Chen Honghui ◽  
Liu Changqin ◽  
Sun Shenggang ◽  
Mei Yuanwu ◽  
Tong E’tang
Keyword(s):  
Cell Surface ◽  
Adhesion Molecules ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Vascular Endothelial

Potential immunosuppressive and antiinflammatory activities of Malaysian medicinal plants characterized by reduced cell surface expression of cell adhesion molecules

2001 ◽  
Vol 15 (8) ◽  
pp. 681-686 ◽  
Author(s):  
Shigeo Tanaka ◽  
Sakata Yoichi ◽  
Lixi Ao ◽  
Mariko Matumoto ◽  
Katsushi Morimoto ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Medicinal Plants ◽  
Cell Surface ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Surface Expression ◽  
Cell Surface Expression

A Cell-Based Adhesion Molecule Bioassay Detects Unexpected Properties of Plasma From Patients with Sickle Cell Disease with Documented Pulmonary Hypertension

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2120-2120
Author(s):  
Antje Ask ◽  
Laurel G. Mendelsohn ◽  
Shoaib Alam ◽  
Alem Mehari ◽  
Caterina Minniti ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cell Adhesion ◽  
Cell Surface ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Heart Catheterization ◽  
Soluble Adhesion Molecules

Abstract Abstract 2120 Pulmonary hypertension (PH) is a common complication in adults with sickle cell disease (SCD) associated with early mortality. Several mechanistic pathways appear to be involved in PH in SCD, one of them being activation of pulmonary endothelium and increased adherence of circulation blood cells. In the past, levels of soluble adhesion molecules in the plasma of patients with SCD have been found to correlate with severity of pulmonary hypertension and risk of mortality. We investigated the association between endothelial-cell based adhesion molecules and markers of PH. We developed a new cell-based ELISA assay and evaluated the induction of cell surface expression of adhesion molecules on cultured microvascular endothelium cells by plasma from subjects with SCD who had undergone right heart catheterization. We found no difference in baseline Intercellular Cell Adhesion Molecule-1 (ICAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) and P-selectin induction by SCD plasma compared to healthy controls. Surprisingly, we found an inverse relationship of cell surface VCAM-1 induction with diagnosis and severity of PH, as indicated by mean pulmonary artery pressure (mPAP) on right heart catheterization. Patients who fell into the upper quartile of VCAM-1 induction had mPAP of 27.6 ± 3.2 mmHg, compared to the middle two quartiles 32 ± 2.3 mmHg, and lower quartile 38.2 ± 4.0 mmHg, (p=0.034). The prevalence of abnormally high pulmonary vascular resistance (>2 standard deviations above the mean) in the high, medium or low VCAM-1 induction groups was 20%, 35% and 80%, respectively (p=0.0066). We also found statistically significant correlations of cell surface VCAM-1 to cardiac output, transpulmonary gradient, pulse pressure, Doppler echocardiography tricuspid regurgitation velocity (TRV) and a marker of systemic iron overload, serum ferritin. Induced cell surface VCAM-1 expression did not correlate significantly in the same subjects with the plasma level of soluble VCAM-1, a previously documented marker associated with high TRV. We found very similar patterns of induction of cell surface expression of P-selectin. These results indicate that the ability of plasma to induce cell surface expression of cell adhesion molecules is a new marker predictive of the diagnosis of catheterization-proven PH in SCD, but it is independent of the levels of the soluble ectodomains of these cell adhesion molecules. These results are consistent with recent publications in the cell adhesion molecule field indicating that independent inflammation-mediated mechanisms regulate adhesion molecule expression and its ectodomain shedding via sheddases. Our findings lead us to speculate that increased sheddase activity may contribute to the high levels of soluble adhesion molecules found in PH, simultaneously reducing the level of cell surface adhesion molecules. Future studies of sheddase activity in SCD PH would help to elucidate this interesting observation. Disclosures: No relevant conflicts of interest to declare.

Prognostic significance of leukopenia at the time of diagnosis in acute myeloid leukemia (AML)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 7070-7070
Author(s):  
M. L. Arellano ◽  
E. Winton ◽  
L. Pan ◽  
L. Souza ◽  
S. Sunay ◽  
...  
Keyword(s):  
Cell Surface ◽  
Adhesion Molecules ◽  
De Novo ◽  
Risk Group ◽  
Statistical Significance ◽  
Univariate Analysis ◽  
Prognostic Significance ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Surface Adhesion

7070 Background: In contrast to the poor prognosis associated with hyperleukocytosis, the prognostic significance of leukopenia at the time of diagnosis of AML is unknown. Methods: Single institution retrospective analysis of 225 consecutive, newly diagnosed AML patients (pts), homogeneously treated between July 1996 and February 2005; and divided into 2 groups based on presenting WBC: < 2,000/uL (30) and > 2,000/uL (195). Simultaneously obtained peripheral blood and marrow blasts were analyzed for cell surface expression of CD34, cKit, CXCR4, PCAM, VLA-2, VLA-3, VLA-4, VLA-5, and FLT3 using flow cytometry. Results: Patients’ characteristics (gender, secondary vs. de novo, and cytogenetic [CTG] risk) were comparable between the 2 groups. Leukopenic AML pts were older (median 56 vs. 53 years, p = 0.02), and had lower induction complete remission [CR] rates: 63% vs. 81% (p = 0.03) by univariate analysis. Induction mortality was 0% for leukopenic and 5% for non-leukopenic pts. In primary refractory pts, median survival was longer for leukopenic (11) vs. non-leukopenic (34) pts: 137 vs. 81 d (p = 0.026). Median follow-up was 22 mos. Event-free (EFS), disease-free (DFS), and overall survivals (OS) were lower in the leukopenic group: 12 vs. 14; 14 vs. 17; and 17 vs. 19 mos, respectively; but did not reach statistical significance. By multivariate analysis, age (p < 0.0001) and CTG risk group (p < 0.0001) were independent predictors of OS, while CTG risk group predicted RFS (p < 0.0001). The level of expression of cell surface adhesion molecules on blood and marrow blasts was comparable for the 2 groups. Conclusions: AML pts presenting with leukopenia have comparable outcomes to those presenting with normal or high WBC despite a lower likelihood of achieving remission. Leukopenic AML did not have over-expression of cell surface adhesion molecules. No significant financial relationships to disclose.

scholarly journals Downregulation of the cellular adhesion molecule Thy-1 (CD90) by cytomegalovirus infection of human fibroblasts

2004 ◽  
Vol 85 (7) ◽  
pp. 1995-2000 ◽  
Author(s):  
Martina Leis ◽  
Manfred Marschall ◽  
Thomas Stamminger
Keyword(s):  
Cell Surface ◽  
Adhesion Molecules ◽  
Human Fibroblasts ◽  
Constitutive Expression ◽  
Surface Expression ◽  
Cellular Adhesion ◽  
Cell Surface Expression ◽  
Gene Products ◽  
E Gene ◽  
Cellular Adhesion Molecule

The deregulation of cellular adhesion molecules by human cytomegalovirus (HCMV) appears to be correlated with the development of vascular disease. In this study, it was investigated whether the expression of Thy-1 (CD90), a member of the immunoglobulin superfamily of adhesion molecules with constitutive expression on fibroblast cells, is modulated following infection with HCMV. It was observed that Thy-1 cell surface expression decreased significantly during the course of infection. Addition of neutralizing antibodies, as well as UV inactivation of virus, prevented Thy-1 downregulation. In contrast, inhibition of virus replication by cidofovir did not alter Thy-1 regulation by HCMV, indicating that immediate-early (IE) and/or early (E) gene products are responsible. Interestingly, after infection of fibroblasts with a recombinant GFP-expressing virus, infected as well as non-infected cells showed a reduced Thy-1 cell surface expression. From these findings, it is concluded that IE or E gene products of HCMV induce a so far unidentified soluble factor that mediates Thy-1 downregulation.

Humic Acid Induces Expression of Tissue Factor by Cultured Endothelial Cells: Regulation by Cytosolic Calcium and Protein Kinase C

1994 ◽  
Vol 71 (03) ◽  
pp. 325-330 ◽  
Author(s):  
Hsin-Ling Yang ◽  
Fung-Jou Lu ◽  
Shu-Li Wung ◽  
Hui-Chong Chiu
Keyword(s):  
Endothelial Cells ◽  
Drinking Water ◽  
Protein Kinase C ◽  
Humic Acid ◽  
Protein Kinase ◽  
Cell Surface ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Vascular Endothelial ◽  
Kinase C

SummaryBlackfoot disease is a thrombotic peripheral vascular disease causally related to the fluorescent humic acid (HA) found in the drinking water of wells in endemic areas in Taiwan. In this study we examined the effect of HA on tissue factor (TF) expression by vascular endothelial cells.Incubation of cultured human umbilical vein endothelial cells (HUVEC) with HA isolated from endemic area drinking water or with a synthetic humic acid polymer (SHA), resulted in enhanced cell surface expression of TF activity by HUVEC. The intracellular calcium level ([Ca24]i) was measured using a calcium-specific fluorescent probe, fura 2. Changes in [Ca24]i level were followed and quantitatively analyzed by spectrofluorometric microscopy, after incubation of the fura 2-loaded HUVEC with HA or SHA in a medium containing 1.8 mM CaCl2. Both HA and SHA increased [Ca2+]i in the presence of extracellular calcium ions, but not in their absence, indicating that influx of extracellular Ca2+ occurred during incubation of HUVEC with HA or SHA. Verapamil, a potent calcium channel blocker, did not abolish the enhancement of [Ca24]i induced by HA or SHA, indicating that specific calcium channels may not be involved in the HA/SHA-induced elevation of [Ca24]i. The elevated [Ca24]i level induced by HA or SHA returned to basal level following removal of HA or SHA and incubation of the washed cells in medium containing 1.8 mM CaCl2. All these changes occurred in the absence of significant cytotoxic effects. The HA/SHA-induced enhancement of cell surface TF activity was inhibited by a specific inhibitor of protein kinase C, H7, suggesting that protein kinase C is involved in the process leading to the enhanced expression of TF activity induced by HA or SHA.In conclusion, this study demonstrates that HA and SHA enhance cell surface expression of TF activity by permeabilization of the cell membrane to extracellular Ca24 ions, leading to elevation of [Ca2+]i that functions as a second messenger to activate protein kinase C, leading finally to enhanced cell surface TF expression. Enhancement of vascular endothelial cell surface TF activity by HA may play a role in the HA-induced thrombotic vascular disorders of Blackfoot disease.

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