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At least 919 records · Page 51Linked to original sources
PubMed2006

Adhesion characteristics of Listeria adhesion protein (LAP)-expressing Escherichia coli to Caco-2 cells and of recombinant LAP to eukaryotic receptor Hsp60 as examined in a surface plasmon resonance sensor.

Listeria adhesion protein (LAP) is an important adhesion factor in Listeria monocytogenes and interacts with its cognate receptor, mammalian heat shock protein 60 (Hsp60). The genetic identity of LAP was determined to be alcohol acetaldehyde dehydrogenase (Aad). A recombinant Escherichia coli strain expressing aad confirmed the involvement of Aad in adhesion to Caco-2 cells. Binding kinetics (ka) of recombinant LAP (rLAP) to Hsp60 was examined in a surface plasmon resonance sensor and was determined to be 5.35 x 10(8) M(-1) s(-1) and it was equivalent to the binding of anti-Hsp60 antibody (ka = 2.15 x 10(9) M(-1) s(-1)) to Hsp60. In contrast, Internalin B, an adhesion/invasion protein from L. monocytogenes, used as a control, had binding kinetics (ka) of only 2.9 x 10(6) M(-1) s(-1). The KD value of rLAP was 1.68 x 10(-8) M, which was significantly lower than Internalin B (KD = 6.5 x 10(-4) M). These results suggest that Hsp60 has significantly higher avidity for anti-Hsp60 antibody and LAP than Internalin B. In summary, LAP is identified as an alcohol acetaldehyde dehydrogenase and binding of recombinant E. coli to Caco-2 cells or rLAP to Hsp60 protein was found to be highly specific.

Adhesins, Bacterial↗
PubMed1978

In vitro adhesion of Escherichia coli to porcine small intestinal epithelial cells: pili as adhesive factors.

Escherichia coli strains with pili (K99 or 987P) known to facilitate intestinal colonization adhered in vitro to porcine intestinal epithelial cells. These strains adhered equally to both ileal and jejunal epithelial cells. A laboratory E. coli strain that has type 1 pili also adhered to porcine intestinal epithelial cells. When nonpiliated cells derived from 987P+, K99+, or type 1 pilus+ strains were used for in vitro adhesion assays, they failed to adhere. The attachment of piliated bacteria to epithelial cells was a saturable process that plateaued at 30 to 40 bacterial cells attached per epithelial cell. Competitive inhibition of bacterial cell attachment to epithelial cells with purified pili showed that only purified 987P competed against the 987P+ strain and only purified type 1 pili competed against the type 1 pilus+ strain. Competition between a K99+ strain and K99 was not consistently achieved. K99+, 987P+, and type 1 pilus+ bacteria could be prevented from adhering to epithelial cells by Fab fragments specific for K99, 987P, or type 1 pili, respectively. Fab fragments specific for non-K99 bacterial surface antigens did not inhibit adhesion of the K99+ strain. It is concluded that adhesion of E. coli to porcine intestinal epithelial cells in vitro is mediated by pili and that the epithelial cells used apparently had different receptors for different pili.

Animals↗
PubMed1993

Role of the CS1 adhesion motif of fibronectin in T cell adhesion to synovial membrane and peripheral lymph node endothelium.

OBJECTIVES: It has previously been shown that the very late antigen-4/vascular cell adhesion molecule-1 (VLA-4/VCAM-1) pathway functions as a receptor/ligand interaction system mediating the recruitment of activated lymphocytes to inflamed synovium of patients with rheumatoid arthritis. This study was performed to determine whether VLA-4 also affects lymphocyte adhesion to inflamed synovium through interaction with the alternatively spliced CS1 domain of fibronectin. METHODS: The effect of the synthetic peptide CS1 on lymphocyte binding to human synovial and peripheral lymph node high endothelial venules (HEVs) was measured in an in vitro frozen section assay. RESULTS: In the presence of the CS1 peptide or antibody to fibronectin, significant inhibition of binding was observed (54 and 51% respectively). Blocking with antibody to VCAM-1 yielded inhibition of binding to 46% of the control value. Maximum inhibition of binding was obtained with a combination of antibody to VCAM-1 and CS1 (65%) and with antibody to VLA-4 alpha (68%). Blocking the classical fibronectin receptor with antibody to VLA-5 alpha gave a slightly lower inhibition at 42%. In normal peripheral lymph nodes, the synthetic peptide CS1 and antibodies to fibronectin and VLA-5 also partially inhibited T cell binding to HEVs (45, 47, and 52% respectively). CONCLUSION: These results show that fibronectin mediates lymphocyte-HEV interactions not only through its classical VLA-5 receptor, but also through its CS1 adhesion motif in inflamed synovium and peripheral lymph nodes.

Arthritis, Rheumatoid↗
PubMed1993

Altered glycosylation of integrin adhesion molecules in colorectal cancer cells and decreased adhesion to the extracellular matrix.

The integrin mediated interactions between tumour cells and the surrounding extracellular matrix are thought to play crucial parts in the complex process of invasion and metastasis. It has been previously shown that the expression of integrins is differently diminished in a chain-specific manner in human colorectal cancer. To further characterise the integrins still expressed in colorectal carcinomas, immunoblots with monoclonal antibodies against the beta 1 integrin subunit have been performed. In isolated cell membranes of colorectal cancers a second smaller beta 1 chain (105 kD non-reduced) was found as well as the mature beta 1 chain (116 kD non-reduced) present in normal mucosa of the colon. This smaller beta 1 chain comigrates with the diminished glycosylated precursor form of the beta 1 chain. The role of N-glycosylation for the function and expression of integrins in vitro was therefore investigated, with deoxymannojirimycin (DMJ) and deoxynojirimycin (DNJ) as specific inhibitors of N-glycan processing. Pretreatment of human colon adenocarcinoma derived HT-29 cells with DMJ resulted in an expression of the 105 kD beta 1 precursor chain and of smaller forms of the alpha 1, alpha 3, alpha 6, and alpha v integrin subunits in a time and dose dependent manner. HT-29 cells treated with DMJ adhered poorly to laminin (8% of untreated controls), collagen type IV (40%), and fibronectin (35%). Pretreatment of the cells with DNJ did not alter the molecular weight of the integrin chains expressed and reduced HT-29 adhesion to laminin and fibronectin only to 68% and 49% respectively. Adhesion to collagen type IV was increased to 124% by DNJ. These results show that N-glycan processing is essential for the function and expression of integrins in human colorectal cancer cells. An altered glycosylation of these adhesion receptors may contribute to a more invasive or metastatic phenotype in colorectal cancer.

Adenocarcinoma↗
PubMed1997

Cell adhesion and migration. I. Neutrophil adhesive interactions with intestinal epithelium.

In many inflammatory conditions of the gastrointestinal tract, disease activity and patient symptoms correlate with the histological finding of neutrophil (PMN) migration across the epithelium. PMN interactions with intestinal epithelium can influence epithelial functions ranging from barrier maintenance to electrolyte secretion. Additionally, PMN recruitment to the epithelium can be modulated by epithelial interactions with luminal enteric pathogens. Adhesive interactions between PMN and intestinal epithelial cells have been shown to be distinct from interactions of PMN with endothelia. In particular, PMN transepithelial migration is modulated by a distinct array of cytokines including interferon-gamma and interleukin-4 and requires the PMN beta2-integrin CD11b/CD18 but is independent of CD11a/CD18, selectins, and intercellular adhesion molecule 1. Additionally, an integral membrane protein termed CD47 has recently been shown to play an important role in PMN transepithelial migration at point(s) subsequent to initial adhesive interactions. This article provides a brief overview of PMN interactions with epithelia and their functional consequences in relation to inflammatory disease.

Animals↗
PubMedDate not supplied

Neural cell adhesion molecule-deficient beta-cell tumorigenesis results in diminished extracellular matrix molecule expression and tumour cell-matrix adhesion.

To understand by which mechanism neural cell adhesion molecule (N-CAM) limits beta tumour cell disaggregation and dissemination, we searched for potential downstream genes of N-CAM during beta tumour cell progression by gene expression profiling. Here, we show that N-CAM-deficient beta-cell tumorigenesis is associated with changes in the expression of genes involved in cell-matrix adhesion and cytoskeletal dynamics, biological processes known to affect the invasive and metastatic behaviour of tumour cells. The extracellular matrix (ECM) molecules emerged as the primary target, i.e. N-CAM deficiency resulted in down-regulated mRNA expression of a broad range of ECM molecules. Consistent with this result, deficient deposition of major ECM stromal components, such as fibronectin, laminin 1 and collagen IV, was observed. Moreover, N-CAM-deficient tumour cells displayed defective matrix adhesion. These results offer a potential mechanism for tumour cell disaggregation during N-CAM-deficient beta tumour cell progression. Prospective consequences of these findings for the role of N-CAM in beta tumour cell dissemination are discussed.

Animals↗
PubMed1993

Histomorphological evaluation of wound healing of rabbit oviduct after microsurgical reanastomosis with the use of autologous fibrin adhesive, human fibrin adhesive or poly-glycolic acid suture.

The morphology of the healing process of microsurgical reanastomosis of the rabbit oviduct with the use of fibrin adhesive, autologous and heterologous, and conventional sutures is described. Both oviducts in 48 rabbits were cut and reanastomosis were performed. The rabbits were killed at different intervals after the operations, ranging from 2 h to 28 days, and the anastomoses were evaluated by histomorphological examination. The autologous fibrin adhesive was absorbed after a week and an uncomplicated healing was observed. Heterologous fibrin adhesive caused a granulomatous inflammation interpreted as an immune reaction of the host to the foreign protein, and conventional suturing resulted in severe tissue damage with an intensive inflammatory reaction.

Animals↗
PubMed1980

Motility and adhesiveness in human neutrophils. Redistribution of chemotactic factor-induced adhesion sites.

Human peripheral blood neutrophils obtained from healthy adults were examined in vitro. We assessed the effects of sequential stepwise increases in the concentration of the chemotactic dipeptide N-formyl-l-methionyl-l-phenylalanine (f-Met-Phe) on neutrophil attachment to serum-coated glass, detachment from serum-coated glass and the distribution on the cell surface of binding sites for albumin-coated latex beads. The initial exposure to f-Met-Phe resulted in increased adhesiveness and binding of latex beads in a random pattern over the cell surface. The second exposure to f-Met-Phe resulted in decreased adherence, detachment of neutrophils from serum-coated glass, and movement of binding sites for latex beads to the uropod. Enhanced adhesiveness and redistribution of binding sites were blocked by 0.1 mM N-alpha-p-tosyl-l-lysine chloromethyl ketone, a concentration that did not reduce the change in cellular shape caused by f-Met-Phe. Cytochalasin B (5 mug/ml) blocked the redistribution of binding sites as well as the change in shape. The third exposure to f-Met-Phe was given along with the latex beads. The stimulus was stopped after 2 min by fixing cells in suspension with glutaraldehyde. If the third exposure was at a concentration higher than the second, the beads were bound in the region of the lamellipodia in 70% of the cells. If lower, binding to the lamellipodia was found in a significantly smaller proportion of cells (13%). The results support the concept that neutrophils develop a polarized distribution of f-Met-Phe-induced adhesion sites in response to increasing concentrations of f-Met-Phe, and these sites flow from the region of the lamellipodia to the uropod.

Adult↗
PubMed1997

Concerted action of tenascin-C domains in cell adhesion, anti-adhesion and promotion of neurite outgrowth.

We used a new approach to identify domains of chicken tenascin-C required for interaction with cells. Instead of expressing the parts of interest, we deleted them from an otherwise intact tenascin-C molecule and scored for the concomitant change in activity. As a starting point for all mutant constructs we expressed the smallest naturally occurring tenascin-C splice variant in vertebrate cells. The tenascin-C mutants had either deletions of all EGF-like repeats, all fibronectin type III repeats or of the fibrinogen globe. In double mutants the fibronectin type III repeats were deleted together with either the EGF-like repeats or the fibrinogen globe, respectively. All tenascin-C variants assembled correctly to hexameric molecules of the expected molecular characteristics. Intact tenascin-C and the mutant missing the fibrinogen globe did not promote adhesion of chick embryo fibroblasts, whereas both, the hexamers containing solely the fibrinogen globe or the EGF-like repeats were adhesive substrates and even supported cell spreading. When tenascin-C was added to the medium of fibroblasts plated on fibronectin-coated wells, cell adhesion was blocked by intact tenascin-C, but not by mutants missing the fibrinogen globe. In neurite outgrowth assays using dorsal root ganglia, processes formed on all substrates except on the mutant missing only the fibrinogen globe, where the ganglia failed to adhere. The mutants missing the fibronectin type III repeats allowed more rapid neurite outgrowth than all other tenascin-C variants and the mutant consisting essentially of oligomerized EGF-like repeats was as active a substrate for neurite outgrowth as laminin. From the combined data, it is concluded that the activities of intact tenascin-C cannot be mimicked by investigating domain by domain, but the concerted action of several domains leads to the diverse cellular responses.

Animals↗
PubMed1987

Effect of patterned surfaces of adhesive islands on the shape, cytoskeleton, adhesion and behaviour of Swiss mouse 3T3 fibroblasts.

A pattern of circular islands of adhesive substratum can be used to control cell shape and behaviour. We have shown previously that the proportion of Swiss 3T3 cells that synthesize DNA varies with the area of the island to which they are attached, within the range 500-5000 microns2. In this paper we investigate the cytoskeleton and adhesions of cells on islands using a variety of techniques including phalloidin staining and interference reflection microscopy. Islands of area 2000 microns2 or less constrain cell shape, and cause focal contacts and actin microfilament bundles to accumulate in a circle at the margin. These changes are most obvious in islands of about 1000 microns2, in which a complete ring of adhesion is sometimes formed in the periphery of the cell. This peripheral distribution is less common in cells on even smaller islands, and the focal contacts become smaller and less numerous. It is not yet clear whether any of these structural changes are associated directly with the proliferative stimulus due to contact with the substratum. However, we expect that the use of patterned substrata will contribute to the study of how cell shape and structure regulate many cell functions.

Actins↗
PubMed2005

Modifier of cell adhesion regulates N-cadherin-mediated cell-cell adhesion and neurite outgrowth.

Modifier of cell adhesion (MOCA) is a member of the dedicator of cytokinesis 180 family of proteins and is highly expressed in CNS neurons. MOCA is associated with Alzheimer's disease tangles and regulates the accumulation of amyloid precursor protein and beta-amyloid. Here, we report that MOCA modulates cell-cell adhesion and morphology. MOCA increases the accumulation of adherens junction proteins, including N-cadherin and beta-catenin, whereas reducing endogenous MOCA expression lowers cell-cell aggregation and N-cadherin expression. MOCA colocalizes with N-cadherin and actin in areas of cell-cell and cell substratum contact and is expressed in neuronal processes. MOCA accumulates during neuronal differentiation, and its expression enhances NGF-induced neurite outgrowth and morphological complexity. We conclude that MOCA regulates N-cadherin-mediated cell-cell adhesion and neurite outgrowth.

Animals↗
PubMed1999

The conveyor belt hypothesis for thymocyte migration: participation of adhesion and de-adhesion molecules.

Thymocyte differentiation is the process by which bone marrow-derived precursors enter the thymus, proliferate, rearrange the genes and express the corresponding T cell receptors, and undergo positive and/or negative selection, ultimately yielding mature T cells that will represent the so-called T cell repertoire. This process occurs in the context of cell migration, whose cellular and molecular basis is still poorly understood. Kinetic studies favor the idea that these cells leave the organ in an ordered pattern, as if they were moving on a conveyor belt. We have recently proposed that extracellular matrix glycoproteins, such as fibronectin, laminin and type IV collagen, among others, produced by non-lymphoid cells both in the cortex and in the medulla, would constitute a macromolecular arrangement allowing differentiating thymocytes to migrate. Here we discuss the participation of both molecules with adhesive and de-adhesive properties in the intrathymic T cell migration. Functional experiments demonstrated that galectin-3, a soluble beta-galactoside-binding lectin secreted by thymic microenvironmental cells, is a likely candidate for de-adhesion proteins by decreasing thymocyte interaction with the thymic microenvironment.

Antigens, Differentiation↗
PubMed1999

Dynamics of astrocyte adhesion as analyzed by a combination of atomic force microscopy and immuno-cytochemistry: the involvement of actin filaments and connexin 43 in the early stage of adhesion.

We observed the time-dependent morphological alteration of astrocytes during their adhesion by atomic force microscopy (AFM) and investigated the relationships between this morphological alteration and the localization of actin filaments and connexin 43 by immunocytochemistry. The fine processes observed as fine ridge-like structures by AFM were closely concerned with actin filaments by immunocytochemistry. During the adhesion of astrocytes, actin filaments appeared to be aligned regularly beyond the borders among different cells. Detectable connexin immunoreactivity was changed in the following regions: 1) the tips of fine cell processes and the cell margin when astrocytes started to adhere; 2) the border of cells when astrocytes tightly adhered; and 3) non-specific sites when astrocytes became a cluster. In the former two cases, the immunopositive spots for connexin were observed to colocalize with the tips of cell processes with actin filaments. These results strongly suggest that connexin associated with actin filaments at the tip of cell processes plays an important role in the early stage of the adhesion of astrocytes. These observations afford valuable clues for understanding the glial communication.

Actin Cytoskeleton↗
PubMed1994

A rapid colorimetric assay for carcinoembryonic antigen (CEA)-mediated cell adhesion and analysis of CEA domains involved in the adhesion.

A colorimetric microadhesion assay that allows the quantitative determination of carcinoembryonic antigen (CEA)-mediated homophilic cell adhesion to CEA immobilized on 96-well polyvinyl chloride plates is described. Chinese hamster ovary (CHO) cells transfected with a full-length CEA cDNA were used as indicator cells. After dislodging nonadherent cells, specifically bound cells were quantified by a colorimetric analysis based on the ability of live cells to reduce the dye 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) to a blue formazan product. The domains of CEA responsible for the homophilic cell adhesion were analyzed by inhibition assays using anti-CEA monoclonal antibodies whose reactive domains were already known. The involvement of domain N and possibly subdomain A3 of CEA in the homophilic cell adhesion has been suggested.

Animals↗
PubMed1996

Cell-adhesion to crystal surfaces. Adhesion-induced physiological cell death.

Cultured epithelial cells interact massively, rapidly and stereospecifically with the ¿011¿ faces of calcium (R,R)-tartrate tetrahydrate crystals. It was suggested that the massive rapid adhesion represents an exaggerated and isolated form of the first initial events in the attachment of cultured cells to conventional tissue culture surfaces (Hanein, et al., Cells and Materials, 5, 197-210; 1995). Attachment is however not followed by normal cell spreading and development of focal adhesions, but results in massive cell death. In this study, the fate of the crystal-bound cells was characterized by electron microscopy, flow cytometry and microscopic morphometry and was found to display the characteristics of physiological cell death. We show that the direct interaction with the highly homogenous and repetitive ¿011¿ faces per se does not trigger the transduction of lethal transmembrane signals. We suggest that the excessive direct interactions between the cell membrane and the crystal, by impairing cell motion, prevent the evolution of RGD-dependent cell adhesion. This implies that the deprivation of proper extracellular matrix (ECM)-receptor contacts of substrate-attached epithelial cells eventually triggers physiological cell death.

Animals↗
PubMed1998

Adhesion of adhesive resin to dental precious metal alloys. Part I. New precious metal alloys with base metals for resin bonding.

New dental precious metal alloys for resin bonding without alloy surface modification were developed by adding base metals (In, Zn, or Sn). Before this, binary alloys of Au, Ag, Cu, or Pd containing In, Zn, or Sn were studied for water durability and bonding strength with 4-META resin. The adhesion ability of the binary alloys was improved by adding In equivalent to 15% of Au content, Zn equivalent to 20% of Ag content, and In, Zn, or Sn equivalent to 5% of Cu content. There was no addition effect of the base metals on Pd, however 15% of In addition improved adhesion with Pd-based alloys containing equi-atomic % of Cu and Pd. The alloy surfaces were analyzed by XPS and showed that oxides such as In2O3, ZnO, or SnO play an important role in improving the adhesive ability of the alloys.

Acrylic Resins↗
PubMed1989

Studies on adhesion to tooth substrate. 6. Adhesion of composite resin to dentin mediated by the dentin primer containing MTYA.

The influences of the kinds and concentrations of the aldehydes in the primer on dentin adhesion were investigated. Moreover, the durability of the adhesion to the dentin treated with primer was examined by thermal cycling tests. Among the aldehyde tested here, glutaraldehyde was effective in improving the adhesion to dentin etched with citric acid. When HEMA was substituted with ethanol, the bond strengths decreased. The relationship between the bond strength and the concentration of glutaraldehyde in the primer was studied. In the cases of phosphoric acid or citric acid etching, the bond strengths were affected by the concentration of glutaraldehyde in the primer. The bond strengths decreased after 2000 thermocycles in phosphoric acid etching.

Adhesiveness↗