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At least 685 records · Page 38Linked to original sources
PubMed1991

Vascular cell adhesion molecule-1 and eosinophil adhesion to cultured human umbilical vein endothelial cells in vitro.

Cultured human umbilical vein endothelial cell (EC) monolayers stimulated with 10 ng/ml tumor necrosis factor demonstrate a time-dependent increase in the expression of the vascular cell adhesion molecule-1 (VCAM-1) with maintained maximal expression at 24 h following EC activation. A monoclonal antibody (mAb) directed against VCAM-1 (1G11) significantly inhibited the adhesion of eosinophils, but not neutrophils, to EC, which had been activated by tumor necrosis factor-alpha for 24 h, but only when eosinophils had been pretreated with an mAb directed against the common beta chain of the CD11/CD18 complex. In the absence of pretreatment with anti-CD18, mAb 1G11 had no significant effect on eosinophil adhesion. These results suggest that eosinophils bind to VCAM-1. However, the functional capacity in this model of the eosinophil receptor for VCAM-1 is likely to be minor compared with the activity of the CD11/CD18 leukocyte adhesion molecules.

Cell Adhesion↗
PubMed1991

The accessory function of murine intercellular adhesion molecule-1 in T lymphocyte activation. Contributions of adhesion and co-activation.

These studies demonstrate that the murine intercellular adhesion molecule-1 (ICAM-1) performs at least two roles in enhancing T cell activation. These two roles are evident in both of our experimental systems: with ICAM-1 expressed on the surface of transfected fibroblast cells, and with purified ICAM-1 immobilized on plastic. First, as has been documented by many investigators, ICAM-1 mediates adhesion between ICAM-1- and lymphocyte function-associated Ag-1 (LFA-1)-bearing cells. This adhesive interaction occurs even in the absence of T cell stimulation, although it is increased by addition of phorbol ester and calcium ionophore. Although ICAM-1 expression does markedly increase intercellular adhesion, the increase is significantly less than the improvement ICAM-1 expression makes in the Ag-presenting ability of MHC class II-transfected fibroblast cells. We have investigated whether this difference is due to LFA-1-mediated signaling, and we present data that demonstrates that although ICAM-1 does not deliver costimulatory signals required for T cell activation, the interaction of LFA-1 with ICAM-1 does synergize with TCR-transduced signals. This synergy is observed for ICAM-1 on live and on chemically fixed accessory cells, and for purified ICAM-1 molecules, but in all cases occurs only when the ICAM-1 and the TCR ligands are on the same surface. Finally, when the ICAM-1 is present on the surface of accessory cells, it enhances T cell activation by changing the Ag dose-dependence of the T cell, but when ICAM-1 and CD3 mAb are co-immobilized, ICAM-1 increases the peak response of the T cell without affecting the dose dependence of the response.

Animals↗
PubMed1994

Involvement of LFA-1/intracellular adhesion molecule-1-dependent cell adhesion in CD40-mediated inhibition of human B lymphoma cell death induced by surface IgM crosslinking.

B cells have been shown to receive negative signals for their growth through crosslinking of surface IgM (sIgM), and it has been demonstrated that anti-IgM Abs induce B cell death. Proliferation of B cells in response to Ag stimulation in vivo may thus require additional signals that inhibit the sIgM-transduced negative signals. Signaling through CD40 has been proposed as a candidate for such costimulatory signals. To investigate the role of CD40-transduced signals in sIgM-mediated B cell death, we used a human B cell line (DND-39) that expresses sIgM, sIgD, and CD40. Crosslinking of sIgM, but not sIgD, by Abs induced DND-39 cell death. The dying cells showed the morphology of apoptosis and DNA fragmentation. Anti-CD40 Abs induced homotypic adhesion of DND-39 cells and rescued them from anti-IgM Ab-induced cell death. Anti-CD40 Abs inhibited anti-IgM Ab-induced cell death when added within 3 h after stimulation with anti-IgM Ab. Treatment with Abs against CD11a, CD18, or CD54 inhibited not only the homotypic adhesion but also the inhibition of anti-IgM Ab-induced apoptosis by anti-CD40 Ab. CD11a antisense decreased the surface CD11a expression, the anti-CD40 Ab-induced homotypic adhesion, and the inhibitory effect of anti-CD40 Ab on anti-IgM Ab-induced apoptosis. The data show that LFA-1/ICAM-1-dependent cell adhesion induced by signaling through CD40 plays an important role in the inhibition of anti-IgM Ab-induced apoptosis of DND-39 cells.

Antigens, CD↗
PubMed1994

Integrin alpha 4 beta 1-mediated melanoma cell adhesion and migration on vascular cell adhesion molecule-1 (VCAM-1) and the alternatively spliced IIICS region of fibronectin.

The integrin receptor alpha 4 beta 1 (also known as VLA-4) binds two different ligands, the endothelial cell surface protein vascular cell adhesion molecule-1 (VCAM-1) and the extracellular matrix component fibronectin. Three distinct sites in fibronectin are recognized by alpha 4 beta 1. Two of these (represented by peptides CS1 and CS5) are present in the alternatively spliced IIICS region and lie in separate, independently spliced segments of this region. A third site resides in the adjacent constitutively expressed HepII domain. Recombinant proteins containing the HepII domain and different splice variants of the IIICS have been generated and compared for their ability to mediate cell attachment, spreading and migration. The activity of these proteins has also been compared with that of a recombinant soluble form of VCAM-1 (rsVCAM-1). All the recombinant proteins supported A375-SM human melanoma cell attachment and spreading in an alpha 4 beta 1-dependent manner, but had varied adhesive activities with rsVCAM-1 > fibronectin variants containing the CS1 sequence >> other fibronectin variants. Low concentrations of rsVCAM-1 and CS1-containing fibronectin variants effectively supported cell migration in a trans-filter assay; however, cell motility was retarded at high concentrations of the same proteins. Fibronectin variants lacking CS1 supported little or no migration. To obtain further insight into the molecular basis of this varied adhesive activity, apparent dissociation constants for each of the recombinant proteins were measured using a solid phase receptor-ligand binding assay. The results revealed a hierarchy of ligand affinities that mirrored their adhesive activity (rsVCAM-1 > fibronectin variants containing CS1 >> other fibronectin variants).

Alternative Splicing↗
PubMed1993

A leukocyte integrin binding peptide from intercellular adhesion molecule-2 stimulates T cell adhesion and natural killer cell activity.

Adhesion is of pivotal importance for a number of leukocyte functions. Little is known about the binding between leukocyte integrins and the intercellular adhesion molecules (ICAMs). Normally integrins are nonadhesive, and require a stimulus to become active. We have now identified a peptide from ICAM-2, which binds to leukocyte integrins and activates adhesion. Furthermore, the peptide strongly increased the binding and cytotoxicity of natural killer cells. These findings show that adhesion-dependent leukocyte functions can be activated by ligand-derived peptides, and therefore provide evidence that the avidity of leukocyte integrins is up-regulated by integrin-ligand interactions.

Alkaloids↗
PubMed1998

Rat neutrophils express alpha4 and beta1 integrins and bind to vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1).

The alpha4 integrins, which are constitutively expressed on all human leukocyte subtypes except neutrophils, interact with vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule (MAdCAM-1) on endothelium to mediate selective recruitment of leukocyte subpopulations, other than neutrophils, to sites of inflammation. However, here we report that a different paradigm of leukocyte recruitment may exist in the rat. Flow cytometric analysis of rat neutrophils using a panel of monoclonal antibodies which recognize rat alpha4 and beta1 integrins showed consistent, low levels of expression. Although alpha4 was expressed at lower levels on neutrophils than all other rat leukocytes, this level of expression was sufficient to mediate significant levels of alpha4- and beta1-dependent neutrophil adhesion to rat and human VCAM-1, and alpha4-dependent, but beta1-independent, adhesion to human MAdCAM-1. These data suggest that rat neutrophils, unlike other species, may use alpha4 integrins to traffic to sites of inflammation in vivo.

Animals↗
PubMed2000

[Adhesive properties of basal membranes of Bruch's membrane. Immunohistochemical studies of age-dependent changes in adhesive molecules and lipid deposits].

BACKGROUND: In addition to deposition of debris between the plasma and basal membrane of the RPE, different types of early and late AMD-like drusen, choroidal neovascularization and pigment epithelial detachments are characterized by splitting of Bruch's membrane between the basement membrane of the RPE and the inner collagenous layer. Because these layers are normally attached by adhesion molecules, the possible age-related regression of these adhesion molecules in this structure was examined. METHODS: The presence of the adhesion molecules laminin, fibronectin, collagen IV and of lipid deposits was examined in 44 macular specimen (age 4-88 years). RESULTS: Age-related regression of the adhesion molecules laminin, fibronectin and collagen IV was observed in the basement membrane of the RPE and the endothelium cells of the choriocapillaris. This effect correlated with an increase in lipid deposits. CONCLUSION: The regression of adhesion molecules, especially in the basement membrane of the RPE in association with increased lipid deposits in Bruch's membrane, may explain the development of a "cleavage edge" for the splitting of Bruch's membrane between the basement membrane of the RPE and the inner collagenous layer.

Adolescent↗
PubMed2006

Improving the performance of EndoRez root canal sealer with a dual-cured two-step self-etch adhesive. I. Adhesive strength to dentin.

This study examined the hypotheses that the use of a self-etching-adhesive improves the adhesion of EndoRez to dentin, and that both techniques are unaffected by the prolonged use of NaOCl when EDTA is used as the final rinse. A tensile bond testing design was employed with composite cylinders bonded to dentin using: (a) 17% EDTA-2 min/EndoRez; (b) 6.15% NaOCl-1 h/EDTA-2min/EndoRez; (c) EDTA-2 min/Clearfil Liner Bond 2V/EndoRez; and (d) NaOCl-1 h/EDTA-2min/Clearfil Liner Bond 2V/EndoRez. Fractographic analyses of debonded specimens were performed using SEM. Two-way ANOVA and Tukey test revealed higher tensile bond strengths with the self-etching-adhesive-modified EndoRez technique (p < 0.001). Sealer tags pulled away from dentinal tubules when EndoRez was used alone, whereas mixed failures occurred within sealer tags, hybrid layers, adhesive, and sealer in the self-etching-adhesive-modified EndoRez technique. Both techniques were unaffected by the prolonged use of NaOCl (p > 0.05) when EDTA was employed as the final rinse.

Analysis of Variance↗
PubMed2005

Adhesion between chemically heterogeneous switchable polymeric brushes and an elastomeric adhesive.

We investigated the adhesive properties of binary heterogeneous polymer brushes made from end-functionalized polystyrene (PS) and poly(2-vinylpyridine) (P2VP) chains. The molecular organization of the mixed brush could be varied reversibly by exposure to selective solvents for PS (toluene) and for P2VP (acidic water). This exposure results in reversible switching of adhesive and wetting properties. The manner in which the adhesion switching occurs can be tuned by the composition of mixed brushes. However, the outer surface composition could be enriched more effectively in PS after the toluene treatment than in P2VP after the acidic water treatment. As a result, the mixed brush compositions that showed the largest difference in properties between an exposure to toluene and an exposure to water were the P2VP-rich compositions. Adhesive properties, tested against a soft hydrophobic pressure-sensitive adhesive (PSA) using a probe test, always showed smaller differences between solvent treatments than wetting properties with water, suggesting a much higher sensitivity of the hydrophobic/hydrophilic brushes to polar molecules than to nonpolar molecules.

Journal Article↗
PubMed2005

[A clinical report of partially debonded adhesion fixed metal splint repaired with adhesion-mechanically fixed metal splint].

PATIENT: The patient was 60-year-old male whose chief complaint was esthetic problem due to median diastema. After orthodontic treatment, an adhesion-fixed metal splint was placed to retain 3-3. After 11 months, the metal retainer on 3 partially debonded. The retainer on 3 was removed and 3 was connected to 4 with an adhesion-mechanically fixed metal splint. Six months later, 3 was separated from 2+2 and connected to 4 5 with the conventional crown restoration. DISCUSSION: The prognosis is good. This result is attributed to the decrease of splint length and the application of the adhesion-mechanical retainer. These seemed to increase the rigidity and prevent deformation of the splint, thus reducing tensile or shear stress applied to the adhesion interface and improving the bonding durability. CONCLUSION: This clinical case suggested that the range of splinting and design of retainer affect the durability of adhesion-fixed metal splints.

Equipment Failure↗
PubMed2000

Adhesive capsulitis of the hip after bilateral adhesive capsulitis of the shoulder.

Adhesive capsulitis of the hip is a not a common clinical presentation. We report a case of adhesive capsulitis of the hip in a patient with hypothyroidism and previous adhesive capsulitis of the shoulder who was receiving thyroid-hormone replacement. The adhesive capsulitis of both hip and shoulder were treated successfully with physical therapy. Orthopedic surgeons should be aware of this diagnosis and its association with shoulder adhesive capsulitis and thyroid dysfunction, to allow them to recognize it and intervene early.

Bursitis↗
PubMedDate not supplied

In vitro attachment to a human cell line of Escherichia coli strains causing urinary-tract infection: occurrence of fimbriae (pili) in adhesive and non-adhesive strains.

In this study, 20 strains of Escherichia coli isolated from infected urinary-tract were screened for the occurrence of haemagglutinating (HA) activity and for the possible relationship between a fimbriate surface structure and adhesion ability to the surface of a human cell line. Only 8 of the 20 adhesive strains agglutinated human or guinea-pig erythrocytes or both. In 7 of the 8 strains, the haemagglutinating activity with human erythrocytes was D-mannose-resistant; one strain was D-mannose-sensitive with guinea-pig red blood cells (RBC). In 40 non-adhering E. coli isolated from urine, D-mannose-resistant HA was rarely detected; in contrast, agglutination of guinea-pig was more frequent and D-mannose-sensitive when it occurred. No correlation was found between the degree of HA activity and the ability to adhere. Moreover at low growth temperature (18 degrees c), haemagglutinin was absent in all the strains tested, whereas residual adhesion capacity could be detected in some strains. Similar results were recorded after heating the bacterial suspension at 65 degrees C. Generally pili detected by electron microscopy were present at the surface of the strains which agglutinated RBC. There is no correlation between the presence of fimbriae or pili and adhesion of E. coli to the human cell line used in this study. A range of distinct mechanisms of E. coli adhesion appeared to be involved in the phenomenon described in this report.

Agglutination↗
PubMed2004

Spatial and temporal sequence of events in cell adhesion: from molecular recognition to focal adhesion assembly.

A new concept that attributes a pivotal role to the pericellular coat in the regulation of the early stages of cell adhesion is presented. Quick, adaptable, and transient adhesion through multiple cooperative weak interactions provides the cell with an additional level of modulation in the decision-making process that precedes the commitment to adhesion at a particular site. Hyaluronan emerges as a modulator of cell adhesion in certain cells, mediating binding or repulsion through its polyelectrolyte character, in addition to its chirality and molecular-recognition properties. The biophysical properties of hyaluronan as well as its ultrastructural organization are analyzed in relation to this proposed function.

Animals↗
PubMed1995

Vascular adhesion molecule-1 and intercellular adhesion molecule-1 expression on rat liver cells after lipopolysaccharide administration in vivo.

During sepsis the infiltration of leukocytes plays a pivotal role in tissue damage. Induction of septic shock results in an early accumulation of polymorphonuclear leukocytes in the liver (after 3 hours), which is followed by an infiltration of mononuclear phagocytes (after 30 hours). Expression of adhesion molecules may contribute to the migration of leukocytes to the site of inflammation. Therefore, in the present study we determined the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) on hepatocytes, liver endothelial cells, and Kupffer cells after lipopolysaccharide (LPS) treatment of rats in vivo. Parenchymal cells showed no constitutive expression of VCAM-1 and the expression could not be upregulated by LPS treatment in vivo, whereas Kupffer and endothelial cells had a low basal expression of VCAM-1 and this expression was increased 40-fold by LPS treatment in vivo. All three cell types showed a basal expression of ICAM-1 and the expression on endothelial liver cells of untreated rats was two times higher than the expression on parenchymal and Kupffer cells. Stimulation with LPS increased the expression of ICAM-1 2.5 times per parenchymal cells and approximately 4 times for endothelial and Kupffer cells. It is concluded that the expression of adhesion molecules may contribute to the influx of leukocytes during septic shock and, therefore, play a role in tissue damage during septic shock.

Animals↗
PubMed1993

Expression of an adhesion molecule and homing in B-cell chronic lymphocytic leukaemia: II. L-selectin expression mediated cell adhesion revealed by immobilized analogue carbohydrates in B-cell chronic lymphocytic leukaemia and monoclonal lymphocytosis of undetermined significance.

The L-selectin mediated adhesion of freshly isolated peripheral blood mononuclear cells (PBMCs) to phosphonomonoester core polysaccharide (PPME) and fucoidin derivatized gels was investigated in seven cases of monoclonal lymphocytosis of undetermined significance (B-MLUS) and 12 cases of chronic lymphocytic leukaemia: B-CLL, patients with peripheral lymphocytosis (LY-patients), lymph node enlargement (LN-patients) and splenomegaly (SM-patients). PBMCs isolated from the peripheral blood of 10 healthy donors served as controls. The binding to PPME and fucoidin correlated well (n = 19, P = 0.01). Adhesion of PBMCs from B-MLUS and B-CLL showed a greater variability than controls. A higher number of cells, on average, bound to PPME and fucoidin derivatized polyacrylamide gels in B-MLUS than in B-CLL. However, the differences observed were not statistically significant. In four cases with B-CLL, the stimulatory effect of interferon-alpha on the function of L-selectin and some other accessory molecules was also studied. The increased binding of PBMCs to immobilized analogue molecules (PPME, fucoidin) and to high endothelial venules (HEVs) in the in vitro HEV-binding assay supports the notion that interferon-alpha not only increases the expression of the adhesion molecules, but also results in an enhanced adhesive function.

Adult↗
PubMed2000

Intercellular adhesion molecular 1 on monocytes mediates adhesion as well as trans-endothelial migration and can be downregulated using antisense oligonucleotides.

The intercellular adhesion molecule 1 (ICAM-1) on endothelial cells is involved in the recruitment of leukocytes to inflammatory sites. In contrast to ICAM-1 expression on endothelial cells, little is known about its function in leukocytes in inflammation. Using ICAM-1-directed anti-sense oligodeoxyribonucleotides (ODNs), we examined the role of ICAM-1 expression on monocytes and lymphocytes for adhesion and trans-endothelial migration. As determined by flow cytometry, a downregulation of the ICAM-1 expression of 50% was observed on peripheral blood mononuclear cells (PBMCs) after their transfection with anti-sense ODNs using cationic lipids. The decrease in the level of ICAM-1 expression in PBMCs was associated with a 36% inhibition of adhesion to interleukin-1beta-stimulated endothelial cells and a 40% reduction of trans-endothelial migration. Gating on particular subsets of the PBMC, the downregulation of ICAM-1 and the functional effects could be ascribed to monocytes, while no significant inhibition was found for lymphocytes. This could be explained by differences in cellular ODN uptake. Since the ligands of ICAM-1 are not expressed on endothelial cells, the results suggest a homotypic interaction among monocytes. In conclusion, in addition to ICAM-1 expression on endothelial cells, ICAM-1 expression on monocytes mediates adhesion and transendothelial migration. This might be relevant for the clinical use of ICAM-1-directed anti-sense ODNs for the treatment of inflammatory diseases, because monocytes appear to be suitable target cells in which to achieve anti-inflammatory effects.

Cell Adhesion↗
PubMed1999

Soluble vascular cell-adhesion molecule-1 and soluble intercellular adhesion molecule-1 correlate with lipid and apolipoprotein risk factors for coronary artery disease in children.

UNLABELLED: Atherosclerosis begins in childhood and progresses from fatty streaks to raised lesions in adolescence and young adulthood. This process is accelerated in children with risk factors for coronary artery disease (CAD). Cell adhesion molecules (CAMs) are supposed to play important roles in the initial development of atherosclerosis, which may suggest that the expression of CAMs is increased in children more than in older subjects or in CAD patients. To determine whether risk factors for CAD are associated with an increased expression of CAMs, we investigated the relationships of the serum levels of soluble vascular cell adhesion molecule-1 (VCAM-1), soluble intercellular adhesion molecule-1 (ICAM-1) and soluble P-selectin (P-selectin) with lipid and apolipoprotein parameters in children (40 boys and 45 girls). We also examined the relationships between soluble CAMs and the fractional esterification rate of cholesterol in HDL (FER(HDL)), particle size of LDL and lipoprotein containing apoA-I, but no apoA-II (LpA-I). In children, soluble VCAM-1 levels were correlated with the levels of triglyceride (in boys) and apoB, the ratio of apoB to apoA-I and FER(HDL) (in girls). Similar associations were found for soluble ICAM-1. Furthermore, the soluble ICAM-1 level was inversely correlated with LpA-I level, LDL size (in boys) and HDL cholesterol level (in girls). Soluble P-selectin levels were not correlated with these parameters. CONCLUSION: Our data indicate that intervention to normalize risk factors for coronary artery disease should be started at a young age to prevent increased expression of cell adhesion molecules.

Adolescent↗
PubMed1986

Hepatocyte adhesion to collagen. Isolation of membrane glycoproteins involved in adhesion to collagen.

Adhesion of hepatocytes to collagenous substrates and their spreading have been shown to involve a specific recognition event, possibly mediated by membrane proteins with affinity for collagen. In the present communication, we describe the isolation of membrane components that are involved in the adhesion of rat hepatocytes to collagen. These components could be solubilized from liver microsomal membranes by treatment with detergents or papain--but not by treatment with EDTA, urea or high salt. The purification of detergent-solubilized components was monitored by an assay determining the ability of membrane components to neutralize antibody-mediated inhibition of hepatocyte adhesion to collagen. By affinity chromatography on lentil lectin-Sepharose it was found that the neutralizing activity resided within the glycoprotein fraction. These glycoproteins were purified further by affinity-chromatography on collagen type I linked to Sepharose. Antibodies raised against the glycoproteins with affinity for immobilized collagen, effectively inhibited hepatocyte adhesion to collagen. The bulk of the neutralizing activity migrated with an apparent molecular weight of 120 000-140 000 in preparative SDS-PAGE.

Animals↗