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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surface phenotypes and adhesion activity to human umbilical vein endothelial cells (HUVECs) were studied using leukemic cells from 12 Japanese patients with B-cell chronic lymphoid leukemias including 7 with chronic lymphocytic leukemia (CLL), 1 with prolymphocytic leukemia (PLL), 2 with hairy cell leukemia (HCL) and 2 with HCL variant (HCL-V). CD13 and CD23 were found to be characteristically positive in CLL, whereas they were not expressed in non-CLL cases except for positivity of CD23 in two such cases. Except for CD11b, all other leukocyte integrins examined (CD11a, CD11c and CD18) and their ligand (CD54) were highly expressed in non-CLL cases. Adhesion activity of leukemic cells to HUVECs after co-culture with HUVECs was well correlated with the expression of CD11b, CD18 and CD54, but showed no predilection for any leukemia subtype. Positivity for CD5, CD21, CD23 and CD13 changed after the co-culture with HUVEC. These results suggest that adhesion activity after co-culture. does not correlate with the leukemia subtype and that endothelial cells activate or differentiate leukemic cells.
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PMID:Surface phenotype and adhesion activity of B-cell chronic lymphoid leukemias. 822 Jan 19

Adhesion between leukemic cells and the vascular endothelium has been suggested to play a role in the development of leukostasis in myelocytic leukemia. To define the role of adhesion molecules on the surface of endothelial cells in leukostasis, we used immunohistochemistry to study the expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in lung tissue of 4 patients with pulmonary leukostasis. Lung tissue of 2 patients with myelocytic leukemia without leukostasis and 4 patients with irrelevant nonpulmonary disease was used as a negative control. Positive control tissues included a lymph node with angioimmunoblastic lymphadenopathy and a hyperplastic tonsil. Weak positive staining for ELAM-1 was found in 1 patient in vessels, both with and without leukostasis. Expression of VCAM-1 and ICAM-1 in all patients tested was similar to that in the negative controls. The results of this study suggest that activation of endothelium, with increased expression of the endothelial adhesion molecules under study, is not a prerequisite for the development of pulmonary leukostasis in leukemia.
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PMID:Endothelial activation antigens in pulmonary leukostasis in leukemia. 823 71

We report a non-HIV patient who had B chronic lymphocytic leukemia (CLL) with progressive multifocal leukoencephalopathy (PML) and diffuse cerebral leukemic parenchymal infiltration in the presence of JC virus and Epstein-Barr virus (EBV) cerebral co-infection. Multiple subcortical hypodensities lining the cortico-subcortical junction were present within the white matter on computerized tomography (CT) scan, with large areas of high signal intensity on T2-weighted sequences on magnetic resonance imaging (MRI). JCV DNA was identified in peripheral blood nuclear cells and cerebrospinal fluid polymerase chain reaction (PCR) DNA/DNA hybridization plus Southern blot analysis. Frontal stereotactic biopsy confirmed the diagnosis of PML by immunocytochemistry, in situ hybridization (ISH) with JC Enzo probe and electron microscopy. Leukemic B cells with the same phenotype as leukemic blood cells were disseminated in the demyelinated areas. They were labeled by anti-latent membrane protein and by BamHl W EBV probe after ISH. Adhesion and activation molecules were positive for CD23. Autopsy showed diffuse visceral leukemic infiltration without acutization. EBV-transformed B lymphocytes would favour JCV penetration and/or intracerebral reactivation of previously latent JCV infection with further development of simultaneous PML and cerebral CLL infiltration in an immunosuppressed patient.
Leukemia 1994 Feb
PMID:Simultaneous progressive multifocal leukoencephalopathy, Epstein-Barr virus (EBV) latent infection and cerebral parenchymal infiltration during chronic lymphocytic leukemia. 830 57

Adhesion under hydrodynamic flow is a step in many complicated physiological processes such as the neutrophil-mediated inflammatory response and cancer cell metastasis. We use a combination of computer simulation and experiment to explore how a population of cells interacts with a ligand-coated substrate under shear flow. To simulate the binding of a single cell to a surface, we use a microvilli-hard sphere model in which receptor-ligand bonds are treated as springs, and the net motion of the cell is determined from a force balance involving hydrodynamic, bonding, and colloidal forces. We show that the adhesive phenotype of a cell depends strongly on the fractional spring slippage of receptor-ligand bonds, which relates the extension of a bond to its rate of breakage; a lower spring slippage indicates bonds can withstand a great deal of extension without a significant increase in the breakage rate, and hence leads to more strongly adherent cells. We construct the behavior of a population of cells by simulating many cells using this algorithm. We show that a homogeneous population of cells with identical numbers of receptors, modeled with parameters suitable to recreate neutrophil rolling, will display a distribution of translational velocities. In addition, we calculate the average velocity for a heterogeneous population of cells which has a Gaussian distribution in receptor number. As the standard deviation of this distribution increases, the average observed velocity for the population increases. Although the homogeneous and heterogeneous populations have the same average number of receptors (10(5)) per cell, there is a significant difference in their average velocity when the standard deviation of receptor number in the heterogeneous population is as little as 25% of the average receptor number. We also present experimental evidence that not all cells exhibit the slow rolling characteristic of neutrophil-endothelial interaction, but rather appear to exist in a "binary" state in which cells are either adherent or noninteracting. We have developed an experimental model system for studying adhesion under hydrodynamic flow, using the rat basophilic leukemia (RBL) derivatized polyacrylamide gels in a flow chamber. Cells are injected into a portion of the flow chamber in which the substrate is not coated with antigen, and allowed to flow over the antigen-coated portion of the gel. We have measured the spatial distribution of cell binding for a population of cells at different flow rates, and have shown that cell binding decreases as shear rate increases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Statistics of cell adhesion under hydrodynamic flow: simulation and experiment. 831 63

We studied the effects of differentiation-inducers on the integrin profile and adhesive properties of K562 leukemia cells. The fibronectin (Fn) receptor integrin, alpha 5 beta 1, was the only integrin expressed in suspension cultured K562 cells. When the cells were exposed to 12-0-tetradecanoylphorbol-13-acetate (TPA) immunoreactivity for the beta 1 integrin subunit was slightly enhanced. TPA exposure also induced the appearance of the alpha 2, alpha 3, alpha v and beta 3 integrin subunits, but the platelet integrin subunit alpha IIb was not detected. On the other hand, hemin chloride-induced erythroid differentiation of K562 cells diminished the expression of the alpha 5 beta 1 integrin on the surface of the cells. Adhesion experiments with TPA-exposed K562 cells indicated that although the adherence to the extracellular matrix (ECM) proteins as a rule was low a few cells spread on these proteins. The present results specify the effects of differentiation inducers on the integrin profile of K562 cells and excludes the comprehension that TPA would induce expression of the platelet integrin alpha IIb on their surface. Our results also show, that an increased expression of a certain integrin does not necessarily lead to a comparable adhesion ability on its ligand in vitro.
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PMID:The effect of differentiation inducers on the integrin expression of K562 erythroleukemia cells. 831 51

Adhesion protein expression by acute myeloid leukaemia (AML) cells may affect bone marrow stromal localization and determine exposure of leukaemic cells to stromal derived myeloid growth factors. We have analysed the surface expression by myeloid leukaemic cells of proteins with known adhesive function and the ability of AML cells to adhere to bone marrow fibroblasts and the extracellular matrix proteins fibronectin and laminin. Cells from all six patients tested adhered to bone marrow fibroblast monolayers (mean binding 28.8 +/- 12.8%) and to purified fibronectin in five cases studied (mean binding 33.8 +/- 15.3%). Cells from four patients with AML also adhered to laminin (mean binding 20.9 +/- 4.0%). AML cells from the majority of patients with leukaemia at diagnosis or relapse expressed the ligand pair LFA-1 and ICAM-1, the CD2 ligand LFA-3, alpha and beta chains of the integrins VLA-4, VLA-5 and VLA-6, and the hyaluronate receptor CD44. Antibodies to CD11a, CD18, VLA-4 alpha, and VLA-5 alpha failed to inhibit binding of AML cells to bone marrow fibroblasts but anti-VLA-5 alpha antibodies inhibited AML cell binding to fibronectin by approximately 50%. The ability of AML cells to adhere to bone marrow fibroblasts and extracellular matrix proteins such as fibronectin and laminin may to help explain the capacity of AML cells to persist in the marrow during periods of apparent complete remission and to subsequently proliferate under the influence of locally secreted myeloid growth factors.
Leukemia 1993 Aug
PMID:Human acute myeloid leukaemia cells express adhesion proteins and bind to bone marrow fibroblast monolayers and extracellular matrix proteins. 835 Jun 18

Adhesion to bone marrow stroma is a key event in normal B lymphopoiesis, allowing exposure of B-cell progenitors to regulatory cytokines. In order to investigate whether similar processes are important in the proliferation of acute lymphoblastic leukaemia (ALL) cells of precursor-B type, the expression of various adhesion molecules was examined. By flow cytometry analysis, CD-44 and the integrins VLA-4 and VLA-5 were the most prominent. CD-44 and VLA-4 were expressed on all 18 cases of precursor-B ALL analysed, while VLA-5 was found on 15 of 18 cases. The integrin CD-11a was detected on 8 of 11 cases, while its ligand, CD-54, was present in 6/12. Other adhesion proteins such as beta 3 integrin, CD-56, CD-15, and Leu8 were not expressed to any significant extent. In view of the known binding of VLA-4 and VLA-5 to extracellular fibronectin (FN), the adhesion of leukaemic cells to FN was evaluated in a colorimetric assay. The precursor-B ALL cell lines REH and KM-3, and 7/15 cases of precursor-B ALL, showed detectable binding to FN. Binding to the other extracellular matrix proteins collagen type 1 and vitronectin was not observed, although two ALL cases showed some binding to laminin. The functional activity of the VLA-4 and VLA-5 molecules was examined using an inhibitory peptide and monoclonal antibodies. These studies indicated that ALL cells adhere to soluble fibronectin predominantly through the VLA-5 molecule (blockable with the PHM-2 antibody and a peptide containing the RGD sequence) although binding mediated by VLA-4 was also apparent in some experiments (blockable by a 40 kDa fragment containing the heparin-binding domain of FN and inhibitory antibodies). These results indicate that precursor-B ALL cells may adhere to marrow stroma through interaction of VLA-4 and VLA-5 with FN, although other mechanisms of adhesion may be important.
Leukemia 1993 Jan
PMID:Adhesion of precursor-B acute lymphoblastic leukaemia cells to bone marrow stromal proteins. 841 84

Cell surface-expressed proteoglycans mediate contacts to extracellular matrix (ECM). Human B lymphocytes produce a species of a proteochondroitin sulfate (CSPG) with an approximate molecular mass of 135-150 kDa. Using a monoclonal antibody (mAb) against B cell CSPG in flow cytometry we found that this CSPG is expressed on tumor cells of patients with CD19+ common acute lymphoblastic leukemia and on the corresponding cell lines Nalm-6, Reh and KM3. The CSPG is also present on hairy cell leukemia JOK-1 cells and weakly on the myeloma line U266. Concomitant with CSPG expression, Nalm-6 cells express the integrins alpha 5/beta 1 (CD49e/CD29) and alpha 6/beta 1 (CD49f/CD29), adhesion receptors for fibronectin and laminin, in contrast to the other two cell lines tested. Expression patterns of these adhesion receptors and CSPG were paralleled by strong adhesion of Nalm-6 to fibronectin and laminin. Adhesion of Nalm-6 to fibronectin was inhibited by the alpha 5-specific antibody SAM 1 by 80% whereas the alpha 6-specific antibody GoH3 reduced binding to laminin only by 20%. A possible involvement of surface-expressed CSPG in adhesion to ECM components was investigated by 24 h incubation of Nalm-6 cells with p-nitrophenyl-beta-D-xyloside, an inhibitor of proteoglycan glycosylation. By this treatment, both adhesion of Nalm-6 to laminin and expression of CSPG were reduced by 40-50%. Furthermore, addition of chondroitin-6-sulfate, a structural element of Nalm-6 CSPG, reduced adhesion of Nalm-6 to laminin by 60%. Chondroitin-4-sulfate, heparin and heparan sulfate did not effectively inhibit the adhesion process. These observations suggest that surface-expressed CSPG may be involved in binding of Nalm-6 cells to laminin and that the specific sulfation pattern of chondroitin-6-sulfate may be essential in this regard.
Leukemia 1996 Jun
PMID:Characterization of cell surface-expressed proteochondroitin sulfate of pre-B Nalm-6 cells and its possible role in laminin adhesion. 866 35

In an in vitro model of monocyte adhesion to glomerular cells, U-937 myelomonocytic leukemia cells irreversibly bind to human mesangial cell monolayers. Adhesion is enhanced in mesangial cells proliferating in response to fetal bovine serum, and in the presence of several cytokines and vasoactive agents. In the present study, co-culture with U-937 followed by removal of non-adherent cells time-dependently decreased viability of mesangial cells, measured either by fluorometry after dual labeling with calcein acetoxymethylester and ethidium homodimer, or by the release of lactate dehydrogenase. The cytotoxic effects of co-culture with U-937 cells were significantly reduced by a combination of free radical scavengers, indicating involvement of reactive oxygen species. U-937 cells also stimulated subsequent proliferation of mesangial cells, assessed by [3H]-TdR incorporation and direct cell counts 24 hours later (from 1,034 +/- 83 to 14,611 +/- 959 and from 2,931 +/- 201 to 19,400 +/- 2,124 cpm/well, quiescent/cycling mesangial cells, respectively, P < 0.01). Controls to rule out TdR incorporation by adherent U-937 cells included selective [3H]-TdR labeling and demecolcine pretreatment. Cell counts at 24 hours confirmed U-937-induced proliferation of quiescent HMC, from 50,575 +/- 3,596 to 143,012 +/- 10,039 cells/cm2 (P < 0.01). Agents that promote U-937 cell adhesion, such as the TxA2 mimetic, U-46619, or angiotensin II, enhanced cytotoxicity while inhibiting the proliferation of both quiescent and cycling mesangial cells, when added during co-culture and the subsequent 24 hours (+1 microM U-46619, 1,875 +/- 131 and 2,546 +/- 125 cpm/well, respectively, 79,793 +/- 5,744 cells/cm2, P < 0.01 vs. U-937 only; +1 microM Ang II, 5066 +/- 560 and 5,784 +/- 306 cpm/well, respectively, 81,068 +/- 4,671 cells/cm2, P < 0.05). Blocking antibodies against the adhesion molecule ICAM-1 and leukocyte counterreceptors (LFA-1, VLA-4) prevented the proliferative response, which could not be duplicated with the conditioned media of U-937 alone or co-cultured with mesangial cells. These findings may reflect the interactions occurring in vivo between infiltrating leukocytes and resident cells during glomerular inflammation.
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PMID:Adhesion of U-937 monocytes induces cytotoxic damage and subsequent proliferation of cultured human mesangial cells. 884 Feb 68

In order to elucidate the involvement of adhesion mechanisms in the process of megakaryocyte-dependent fibroblast growth, we applied BSA-coupled polymers of glucose, galactose, fucose, mannose, and several lectins (AAA, LCA, LTA, UEA-I) to cocultures of CD61 -positive (CD61+)/MACS-enriched megakaryocytes and human bone marrow fibroblasts. Fibroblast monocultures served as controls. After 6 days, glucose, as well as galactose-treated cultures showed a significant reduction of fibroblast growth in cocultures and fibroblast monocultures. In contrast, application of mannose caused no reducing effect on fibroblast numbers. Administration of fucose, AAA, LTA or UEA-I revealed a strong impairment of fibroblast growth in the megakaryocyte-fibroblast cocultures. Adhesion experiments using MACS-enriched, fluorescein-labelled megakaryocytes cultured in the presence of carbohydrates and lectins on a near-confluent layer of fibroblasts were additionally performed. Following fucose-BSA, alpha Fuc-1,2Gal beta-HSA or UEA-I treatment a significant reduction of megakaryocyte adhesion to the fibroblast layer could be observed. In the case of AAA a weak impairment of megakaryocyte adhesion could be noticed. Selective pretreatment of either fibroblasts or megakaryocytes with fucose-BSA or alpha Fuc-1,2Gal beta-HSA was consistent with the finding of a prominent involvement of fucosylated residues located on megakaryocytes in this interaction. In conclusion, our studies are in keeping with the assumption that fucosylated and fucose-binding structures are playing a key role in adhesion mechanisms between megakaryocytes and fibroblasts and thus influence significantly the megakaryocyte-dependent growth of bone marrow fibroblasts.
Leukemia 1996 Oct
PMID:Interactions between endogeneous lectins and fucosylated oligosaccharides in megakaryocyte-dependent fibroblast growth of the normal bone marrow. 884 95


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