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Vascular cell adhesion molecule-1 and VLA-4 are obligatory adhesion proteins in the heterotypic adherence between human leukemia/lymphoma cells and marrow stromal cells.

We have utilized two well-characterized human leukemia/lymphoma (LL) cell lines, UTMB-460 and CEM, to determine the role of integrin very late antigen-alpha 4 beta 1 (VLA-4) and its ligand vascular cell adhesion molecule-1 (VCAM-1) in the adherence of the LL cells to marrow stromal cells (MSC). Both these LL cell lines express alpha and beta subunits of VLA-4. VCAM-1 is constitutively expressed by human MSC and its expression can be upregulated by interleukin-4 (IL-4) and recombinant human tissue necrosis factor-alpha (rTNF-alpha). IL-4 and rTNF-alpha stimulation of MSC is associated with a significant increase in the adherence of both UTMB-460 and CEM LL cells to the cytokine-stimulated MSC. Monoclonal antibodies directed against the alpha and beta subunits of VLA-4 and VCAM-1 significantly inhibit adherence of the LL cells to unstimulated and cytokine-treated MSC. The data reported indicate that VCAM-1 and integrin VLA-4 are obligatory adhesion proteins in the heterotypic adherence between human LL cells and MSC. The constitutive expression of VCAM-1 by MSC may be partially responsible for retention of leukemia cells in th bone marrow and metastasis of lymphomas to the bone marrow.

Antibodies, Monoclonal↗

Interfacial and surface characterization of two self-etching adhesive systems and a total-etch adhesive after bonding to ground and unground bovine enamel--a qualitative study.

The purpose of the study was to evaluate the enamel surface and interface morphology of two self-etching adhesive systems (SAS) vs a total-etch control, after bonding to ground and unground enamel using field emission scanning electron microscopy (FESEM). Thirty bovine incisors were used in this study. The buccal enamel surface of 15 teeth was ground flat to resemble freshly cut enamel. The rest of the teeth were left intact. Two SAS, Clearfil SE Bond (CSE, Kuraray) and Prompt L-Pop (3M-ESPE), and a conventional adhesive system, Scotchbond Multipurpose (3M-ESPE, control), were used to condition the surface of unground and ground enamel on 12 teeth. A composite button was bonded to the remaining 18 teeth; a cross-section (1 mm thick) was obtained from each and the bonded interface was polished. All specimens were dehydrated in ascending grades of ethanol, gold-sputter-coated, and observed under FESEM (Hitachi S-4000) to evaluate the ultrastructural morphology of the enamel surface and the enamel-dentin interface. The etching patterns and adhesive penetration varied according to the aggressiveness of the SAS, with CSE being the mildest and H3PO4 being the most aggressive. There were no significant differences on the ultrastructural morphology of the enamel surface between unground and ground specimens. It appears that microporosities within enamel prisms provide sufficient enamel-resin hybridization in unground enamel. The enamel dissolution pattern and depth of infiltration depend on the type of SAS used, with no significant differences in unground and ground enamel.

Animals↗

Correlation of in vivo and in vitro performance of adhesive restorative materials: a report of the ASC MD156 Task Group on Test Methods for the Adhesion of Restorative Materials.

Before a standard designed to test the adhesion of adhesive restorative materials can be accepted, it is necessary to identify those parameters which are of clinical relevance and which can be studied under in vitro testing conditions. The goal of this report has been to identify information related to how dentinal fluid, intra-tubular pressure, polymerization shrinkage, cavity preparation, cavity shape, placement technique, curing method, tooth age, environmental conditions, masticatory forces, thermal cycling, and microleakage influence the bond strength++ of adhesive restorative materials. This review is also intended to function both as an information base of past experimental data as well as a source of guidance for further, needed research.

American Dental Association↗

A smart adhesive joint: entropic control of adhesion at a polymer/metal interface.

The study of adhesion has a long and rich history, with theory, experiments, and applications bridging numerous disciplines, including physics, chemistry, engineering, and medicine. This diverse interest has led to the development of a large number of methods for both enhancing and inhibiting adhesion at specific interfaces of interest. We report herein "smart" adhesion at a polymer/metal (oxide) interface that responds reversibly to changes in temperature by increasing or decreasing in magnitude. The temperature dependence in this system arises from the rubber elasticity of the polymer, 1,4-polybutadiene, and mirrors the interfacial behavior of the same polymer against water. Such systems offer unique opportunities for designing responsive materials whose properties can be actively controlled.

Journal Article↗

Computational studies on polymer adhesion at the surface of gamma-Al2O3. I. The adsorption of adhesive component molecules from the gas phase.

We calculate the minimum energy paths and reaction energies of the adsorption of the epoxide adhesive components diglycidylesterbisphenol A (DGEBA), diethyltriamine (DETA), and the adhesion promoter 3-aminopropylmethoxysilane (AMEO) at two different sites on a model of the native Al2O3 surface, using the nudged elastic band algorithm in conjunction with self-consistent charge-density functional based tight binding. Our results show that the chosen combination of methods is well suited to obtain an overview of the reaction mechanisms and kinetics of the adsorption of organic molecules on inorganic surfaces. The obtained MEP-s show that there is preference for the adsorption of the adhesion promoter, AMEO, over the resin, DGEBA, while the adsorption of the curing agent, DETA, is unfavorable. Our approach also gives an insight into the ranges of the mechanical and electronic influences of the adsorption process on the interface, which neither full ab initio methods nor force field approaches can provide. These results will help to develop a quantum mechanics-molecular mechanics multiscale embedding scheme for more detailed studies of organic/inorganic hybrid interface reactions.

Journal Article↗

Adhesion to root canal dentine using one and two-step adhesives with dual-cure composite core materials.

The regional tensile bond strengths of two dual-cure composite resin core materials to root canal dentine using either a one or two-step self-etching adhesive were evaluated. Extracted premolar teeth were decoronated and their root canals prepared to a depth of 8 mm and a width of 1.4 mm. In one group, a one-step self-etching adhesive (Unifil Self-etching Bond) was applied to the walls of the post-space and light-cured for 10 s. After which, the post-spaces were filled with the a dual-cure composite resin (Unifil Core) and then half the specimens were light-cured for 60 s and the other half placed in darkness for 30 min. In the second group, a self-etching primer (ED Primer II) was applied for 30 s, followed by an adhesive resin (Clearfil Photo Bond), which was light-cured for 10 s. The post-spaces were filled with a dual-cure composite resin (DC Core) and then half the specimens were light-cured for 60 s and the other half placed in darkness for 30 min. Chemical-cure composite resin was placed on the outer surfaces of all the roots, which were then stored in water for 24 h. They were serially sliced perpendicular to the bonded interface into 8, 0.6 mm-thick slabs, and then transversely sectioned into beams, approximately 8 x 0.6 x 0.6 mm, for the microtensile bond strength test (muTBS). Data were divided into two (coronal/apical half of post-space) and analysed using three-way anova and Scheffe's test (P < 0.05). Failure modes were observed under an scanning electron microscope (SEM) and statistically analysed. Specimens for observation of the bonded interfaces were prepared in a similar manner as for bond strength testing, cut in half and embedded in epoxy resin. They were then polished to a high gloss, gold sputter coated, and after argon ion etching, observed under an SEM. For both dual-cure composite resins and curing strategies, there were no significant differences in muTBS between the coronal and apical regions (P > 0.05). In addition, both dual-cure composite resins exhibited no significant differences in muTBS irrespective of whether polymerization was chemically or photoinitiated (P > 0.05). Both dual-cure composite resins exhibited good bonding to root canal dentin, which was not dependent upon region or mode of polymerization.

Bicuspid↗

Adhesive solutions: report of a case using multiple adhesive techniques in the management of enamel hypoplasia.

Enamel hypoplasia is a common condition that may present a severe aesthetic problem. Although the teeth affected may not be particularly susceptible to caries, patients may request cosmetic improvement. Adhesive techniques may be useful in such situations. This paper discusses the management of a patient with enamel hypoplasia using a combination of adhesive systems including enamel- and dentine-bonded veneers, dentine-bonded crowns, a cantilever resin-retained bridge, bonded amalgam restorations and chairside tin plating. Where adhesion was contraindicated, conventionally retained crowns were used.

Adult↗

A peptide corresponding to GPIIb alpha 300-312, a presumptive fibrinogen gamma-chain binding site on the platelet integrin GPIIb/IIIa, inhibits the adhesion of platelets to at least four adhesive ligands.

The platelet fibrinogen (Fg) receptor (GPIIb/IIIa) is an integrin which plays a critical role in hemostasis by recognizing at least the four adhesive ligands: Fg, fibronectin (Fn), vitronectin (Vn), and von Willebrand factor (vWf). We reported that residues 309-312 of GPIIb alpha appear to comprise at least part of a Fg binding site on the Fg receptor (Gartner, T. K., and Taylor, D. B. (1990) Thromb. Res. 60, 291-309). Here we report that the peptide GPIIb alpha 300-312 (G13) inhibits platelet aggregation and binds Fg and Vn. Significantly, this peptide inhibits the adhesion of stimulated platelets to Fg, Fn, Vn, and vWf, but not the adhesion of resting platelets to Fn. Thus, GPIIb 300-312 may constitute a specific but common recognition site on GPIIb/IIIa for both LGGAKQAGDV- and RGD-containing ligands.

Amino Acid Sequence↗

Cloning and functional characterization of DSCAML1, a novel DSCAM-like cell adhesion molecule that mediates homophilic intercellular adhesion.

DSCAM, a conserved gene involved in neuronal differentiation, is a member of the Ig superfamily of cell adhesion molecules. Herein, we report the functional characterization of a human DSCAM (Down syndrome cell adhesion molecule) paralogue, DSCAML1, located on chromosome 11q23. The deduced DSCAML1 protein contains 10 Ig domains, six fibronectin-III domains, and an intracellular domain, all of which are structurally identical to DSCAM. When compared to DSCAM, DSCAML1 protein showed 64% identity to the extracellular domain and 45% identity to the cytoplasmic domain. In the mouse brain, DSCAML1 is predominantly expressed in Purkinje cells of the cerebellum, granule cells of the dentate gyrus, and in neurons of the cerebral cortex and olfactory bulb. Biochemical and immunofluorescence analyses indicated that DSCAML1 is a cell surface molecule that targets axonal features in differentiated PC12 cells. DSCAML1 exhibits homophilic binding activity that does not require divalent cations. Based on its structural and functional properties and similarities to DSCAM, we suggest that DSCAML1 may be involved in formation and maintenance of neural networks. The chromosomal locus for DSCAML1 makes it an ideal candidate for neuronal disorders (such as Gilles de la Tourette and Jacobsen syndromes) that have been mapped on 11q23.

Animals↗

An ICAM-1 like cell adhesion molecule is responsible for CD34 positive haemopoietic stem cells adhesion to bone-marrow stroma.

The microenvironment in the haematopoietic organs plays an important role in regulating and sustaining differentiation and self-renewal of haematopoietic stem cells. Although crucial for stem cell maintenance and homing, the stromal cell-stem cell interactions are poorly understood. Here we show that an ICAM-like molecule is responsible for stem cell adhesion to stromal cells in vitro. The molecule was characterized by a monoclonal antibody 3E10. Immunoblotting results indicated that the molecule had an electrophoretic mobility equal to that of intercellular cell adhesion molecule-1 (ICAM-1). Binding inhibition assays, however, showed that inhibition of binding of enriched CD34 cells by 3E10 was more prominent in comparison with that of ICAM-1.

Antibodies, Monoclonal↗

Soluble intercellular adhesion molecule-1 (ICAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1), and tumor necrosis factor receptor (55 kDa TNF-R) in patients with acute Plasmodium falciparum malaria.

Adhesion of Plasmodium falciparum-infected erythrocytes to vascular endothelium is in part mediated by ICAM-1 and ELAM-1 (E-selectin), which can be induced via the 55-kDa TNF-receptor (TNF-R55kDa). We have studied serum levels of soluble ICAM-1 (sICAM-1), ELAM-1 (sELAM-1), and soluble TNF-R55kDa (sTNF-R55kDa) in 37 patients with uncomplicated P. falciparum infection and in 17 control subjects in Bangkok, Thailand. The serum levels of sICAM-1 were markedly elevated in patients prior to treatment (601 +/- 239 ng/ml versus 160 +/- 47 ng/ml in healthy controls). In addition, elevated levels of sELAM-1 (53.6 +/- 23.1 ng/ml versus 21.5 +/- 10.1 ng/ml) and sTNF-R55kDa (4.7 +/- 3.2 ng/ml versus 1.0 +/- 0.4 ng/ml) were observed (P < 0.05 for all). Soluble ELAM-1 reached normal levels on Day 3, and sTNF-R55kDa on Day 14, while sICAM-1 was still significantly elevated 28 days after treatment was started (P < 0.05 for all). A correlation between sTNF-R55kDa (P < 0.05) and sELAM-1 (P < 0.05), respectively, with parasitemia prior to antimalarial treatment was found. These results suggest that a TNF-mediated expression of adhesion molecules induced by the asexual stage of malaria parasites serves as an immune-evasion mechanism.

Acute Disease↗

The cell adhesion molecule retina cognin is a cell surface protein disulfide isomerase that uses disulfide exchange activity to modulate cell adhesion.

The retina cell adhesion molecule, R-cognin, shares cDNA sequence with protein disulfide isomerase (PDI) but has a different molecular size and subcellular location. We asked whether R-cognin originated from a unique PDI gene transcript or was a product of posttranscriptional processing. The 3'-terminal partial cDNA clone for R-cognin was extended by both 5' RACE and by PCR from sequence near the 5' end of the PDI-translated region. The cDNA sequence was compared to those of chicken, bovine, and human PDI. The R-cognin cDNA sequence was identical to that of chicken PDI and differed by less than 10% from mammalian PDI proteins. The role of the disulfide exchange activity characteristic of both proteins was studied by assessing the cell-aggregation-enhancing ability and tissue specificity of R-cognin and recombinant human PDI and its derivatives. Chicken and normal human PDI proteins showed tissue- and developmental-specific enhancement of cell aggregation identical to R-cognin, and this activity was blocked by inactivation of the -WCGHC- motifs which function in disulfide exchange. Dependence of retina cell aggregation on disulfide exchange activity was shown by blocking that activity with the inhibitor, DTNB, or with a recombinant human PDI with the -WCGHC- motif cysteines mutated. The results suggest that one -WCGHC- motif in R-cognin is sufficient and that the more C-terminal motif is most active. We conclude that R-cognin is a tissue-specific protein product of the standard PDI chicken gene. The -WCGHC- motif in mature R-cognin is necessary, but not sufficient, for cell adhesion.

Amino Acid Sequence↗

Carcinoembryonic antigen (CEA) and CEA-related cell adhesion molecule 1 (CEACAM1), apically expressed on human colonic M cells, are potential receptors for microbial adhesion.

In the human gut mucosa, specialized M cells deliver intact foreign macromolecules and commensal bacteria from the lumen to organized mucosal lymphoid tissues triggering immune responses. M cells are also major sites of adhesion and invasion for enteric pathogens. The molecular features of M cell apical surfaces that promote microbial normal attachment are still largely unknown. We have demonstrated previously that in the human colonic epithelium, carcinoembryonic antigen (CEA) and CEA-related cell adhesion molecule 1 (CEACAM1) are integral components of the apical glycocalyx which participate in epithelial-microbial interactions. In this study, based on the reactivity of specific monoclonal antibodies and on immunoelectron microscopy, we show that M cells of human colonic solitary lymphoid follicles express CEA and CEACAM1 on the apical surface. Recently these highly glycosylated molecules have been characterized as protein receptors for different bacteria. This leads us to propose a role for CEA and CEACAM1 in the adherence of enteric bacteria to the apical membrane of colonic M cells. We also hypothesize that, unlike colonic enterocytes, M cells lack the defense mechanism that eliminates CEA and CEACAM1 upon microbial binding and which is based on vesiculation of microvillus plasma membrane.

Antigens, CD↗

Neural cell adhesion molecule (NCAM) in adult vertebrate retinas: tissue localization and evidence against its role in retina-pigment epithelium adhesion.

The presence of neural cell adhesion molecule (NCAM) was examined in the neural retina, interphotoreceptor matrix (IPM), and retinal pigment epithelium (RPE) of adult bovine and frog eyes. Using polyclonal antibodies raised against adult isoforms of NCAM. Western blot analyses revealed the presence of NCAM in the neural retina, but not in the IPM or RPE of these species. As a control, Western blot analysis was used to demonstrate the presence of interphotoreceptor retinoid-binding protein (IRBP) in the IPM preparations. NCAM immunoreactivity was detected by light microscopic immunocytochemistry primarily in the plexiform layers and nerve fibre layer of the frog retina. Minor immunoreactivity was also detected in the inner and outer nuclear layers, but there was no detectable NCAM immunoreactivity in the IPM, outer segments, or RPE. These results indicate that NCAM is not a likely participant in the process of retina-RPE adhesion in the adult eye.

Animals↗

Intercellular adhesion molecule-1, intercellular adhesion molecule-3, and leukocyte integrins in leukocyte accumulation in membranoproliferative glomerulonephritis type I.

Marked intraglomerular infiltration of leukocytes is observed in membranoproliferative glomerulonephritis (MPGN). We recently demonstrated that this leukocyte infiltration develops partly through macrophage-1 (Mac-1)-positive cells and glomerular C3c deposits (Clin Exp Immunol 100:269-276, 1995). To further investigate the mediation of adhesion molecules in the leukocyte accumulation, we immunohistochemically examined the expression of intraglomerular leukocyte integrins and their ligands as well as surface markers for granulocytes/monocytes (CD15) and macrophages (CD68) in 26 patients with MPGN type I who had undergone repeated biopsies. These patients were divided into two groups. Group A included the patients who showed both normo-complementemia and urinary protein excretion less than 1 g/d at the follow-up biopsy (recovery group: n = 14). Group B (persistent group: n = 12) included the patients other than those in group A. At the initial biopsy, there was no difference in the degree of glomerular C3c deposition, glomerular intercellular adhesion molecule (ICAM)-1 expression, or the numbers of cells bearing leukocyte function-associated antigen-1 (LFA-1), Mac-1, and ICAM-3 between the two groups. At the follow-up biopsy, the degree of glomerular C3c deposition, and the numbers of cells bearing LFA-1, Mac-1, and ICAM-3, were significantly decreased only in group A (P < 0.01, P < 0.001, P < 0.001, and P < 0.01, respectively). No chronological change in ICAM-1 expression was observed in either group. Group B showed a chronological increase in the severity of glomerular injury and serum creatinine level, associated with persistent heavy proteinuria. Neither LFA-1- nor Mac-1-positive cells were positively correlated with ICAM-1 expression. Most of Mac-1-positive cells were CD15-positive cells (granulocytes/monocytes), and a considerable number of Mac-1-positive cells concurrently expressed ICAM-3. In contrast, most LFA-1-positive cells were considered to be CD68-positive cells (macrophages). The number of cells bearing LFA-1 was positively correlated with that of cells bearing ICAM-3 (P < 0.00001). These results suggest that the glomerular leukocytes, infiltrating through Mac-1/complement interaction, express ICAM-3 by themselves, and that LFA-1/ICAM-3 interaction might participate in the glomerular aggregation of leukocytes in MPGN type I. In this study, we could not conclude that LFA-1/ICAM-1 or Mac-1/ICAM-1 interaction was involved in the leukocyte accumulation in this disease.

Adolescent↗

Regulation of E-kinase mediated cell-adhesion molecule(s) function by E-NTPase(s): imminent regulatory inter-dependency for cell adhesion.

E-NTPase is a cell membrane bound enzyme, suggested to play a role in maintaining the [NTP](o) and cell adhesion. Attempts to purify this enzyme resulted identification of many proteins co-purifying with E-NTPase. The amino acid sequence of chicken gizzard smooth muscle E-NTPase has been shown to have considerable amino acid sequence homology with mammalian CD39. On the other hand, the purified rat cardiac sarcolemmal E-NTPase showed identical sequence homology with platelet CD36. In this communication, an effort was made to provide rationale for the functional relevance of E-NTPase with reference to cell-adhesion process.

Adenosine Triphosphatases↗

Effects of remifentanil on neutrophil adhesion, transmigration, and intercellular adhesion molecule expression.

BACKGROUND: Anaesthetic drugs are used for pain therapy and anaesthesia. Neutrophils play a significant role during the process of inflammation. The aim of the current study was to investigate the effects of remifentanil and fentanyl on neutrophil migration through endothelial cell monolayers, and on adhesion molecule expression. METHODS: After isolation of polymorphonuclear neutrophils (PMNL) we used a currently described migration assay. PMNL and/or endothelial cell monolayers (ECM) were pre-treated with remifentanil using clinically relevant, as well as higher and lower concentrations or relevant concentrations of fentanyl. RESULTS: Concentrations of remifentanil (50 ng/mL) similar to the relevant plasma concentration were able to inhibit PMNL migration through ECM significantly (migration compared to the control 82+/-7% SD; P<0.05), when both cell types were treated with the synthetic narcotic remifentanil. Fentanyl (30 ng/mL) showed a stronger inhibitory effect (migration compared to the control 67+/-9.2%; P<0.05). Endothelial cell adhesion molecule expression was reduced after either remifentanil or fentanyl. CONCLUSION: The results of the present investigation indicate that remifentanil influences interaction of ECM against human neutrophils. Compared to fentanyl, remifentanil seems to exhibit minor inhibitory effects on neutrophil migration.

Analgesics, Opioid↗

Roles of immunoglobulin-like loops of junctional cell adhesion molecule 4; involvement in the subcellular localization and the cell adhesion.

BACKGROUND: Membrane-associated guanylate kinase with inverted domain structure-1 (MAGI-1) is a scaffolding protein at tight junctions (TJs). We have recently identified junctional adhesion molecule 4 (JAM4) as a MAGI-1-interacting protein. JAM4 belongs to the immunoglobulin superfamily and mediates Ca2+-independent adhesion. In this study, we examined the subcellular localization of JAM4 in various tissues and the involvement of JAM4 in the localization of MAGI-1. Moreover, we investigated into roles of immunoglobulin-like loops (Ig-loops) of JAM4. RESULTS: JAM4 was localized at TJs but also on apical membranes of epithelial cells in jejunum, ileum, and renal proximal tubules. In Madine Darby canine kidney (MDCK) cells, the localization of JAM4 at TJs depended on the first Ig-loop and did not require the MAGI-1-interacting region. JAM4 determined the subcellular localization of MAGI-1 in MDCK cells. In ileum, however, MAGI-1 was localized at TJs where JAM4 was not detected. Both of Ig-loops were necessary for homophilic interactions, but cis interactions depended on the first Ig-loop. CONCLUSION: JAM4 may be primarily targeted to apical membranes, and subsequently recruited to TJs through the first Ig-loop-mediated molecular interaction. JAM4 determines the localization of MAGI-1 in MDCK cells, but the in vivo localization of MAGI-1 does not necessarily depend on JAM4.

Animals↗