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PubMed2005

An elastic-plastic hybrid adhesion model for contacting rough surfaces in the presence of molecularly thin lubricant.

The study of adhesion has received considerable attention in recent years, partly due to advances in the design and fabrication of micro/nano devices. Many adhesion investigations are centered on single-spherical-contact models, which include the classic Johnson-Kendall-Roberts (JKR), improved Derjaguin-Muller-Toporov (IDMT), and Maugis-Dugdale (MD) models. Based on the IDMT single-asperity model, adhesive rough surface contact models have also been developed, which are valid for elastic and elastic-plastic contact conditions. A limitation of the IDMT-based models is that they are only valid for application cases with low adhesion parameter values. In this research, a contacting rough surface adhesion model was developed by combining an extended Maugis-Dugdale (EMD) model (which is only valid for elastic contacts) with an IDMT-based elastic-plastic adhesion model. The proposed model, termed the elastic-plastic hybrid adhesion model, is valid for the entire adhesion parameter range and also for elastic-plastic contacts. The proposed model gives results similar to the EMD rough surface model when the contact is primarily elastic. Moreover, the proposed model was compared to an IDMT-based model (ISBL model) and both gave similar results for contacts with low adhesion parameter values. With high adhesion parameter values, the ISBL model fails, whereas the proposed model correctly predicts higher adhesion. Last, based on the stiffness of the external force, the instability for adhesive rough surfaces in contact was also discussed, and it was postulated that a high peak value of the external force stiffness directly relates to the unstable contact process.

Journal Article↗
PubMed1998

Expression of 32/67-kDa laminin receptor in laminin adhesion-selected human colon cancer cell lines.

Laminin promotes the malignant phenotype, and the expression of certain laminin receptors is increased in malignancy. Previously, we demonstrated that a laminin-adhesive subclone of a human colon cancer cell line showed increased tumorigenicity in nude mice and increased affinity of the beta1 integrin for laminin relative to the laminin-non-adhesive subclone. The total amount of either beta1 integrin protein or mRNA did not increase. As levels of the 32/67-kDa laminin receptor (67LR) correlate with malignancy, we examined 67LR expression in the laminin adhesion-selected human colon cancer cells. The laminin-adhesive subclone, which was more tumorigenic in both heterotopic and orthotopic locations than in a laminin-non-adhesive subclone, showed cell-surface membrane staining of 67LR, whereas the laminin-non-adhesive subclone showed cytoplasmic staining of 67LR. No difference in either the amount of 67LR mRNA or the amount of protein was observed in the parental cells than in the laminin-adhesive and non-adhesive subclones. When assayed on a laminin affinity column, more 67LR molecules bound to the column with cell extracts from the laminin-adhesive subclone than was observed with the non-adhesive subclone. These findings suggest that the increased tumorigenicity of laminin adhesion-selected tumour cells might be due to an alteration in the distribution and/or adhesiveness of multiple receptors including 67LR and beta1 integrin.

Animals↗
PubMed1981

Strategies for specifying form and pattern: adhesion-guided multicellular assembly.

We define a material pattern as a particular arrangement of material elements in space. We then make an effort to categorize the developmental strategies that underlie the emergence of multicellular patterns. These strategies are divided into three broad categories according to whether cell position influences or is influenced by cell fate. In that category of strategies in which cell fate influences cells to move to particular positions, we focus our attention upon morphogenetic and patterning phenomena that appear to be determined by adhesion-mediated interactions of cells with each other and with their surroundings. The differential adhesion hypothesis details how cellular adhesive properties can guide tissue movements and specify patterns of cell association. Motile, adhesive cells will naturally tend to group so as to maximize their adhesive interactions (minimize interfacial free energy). A homogeneous population of uniformly adhesive (isotropic) cells will tend toward spherical form. Cell surface adhesive anisotropies can determine other most-stable (equilibrium) configurations of the population, such as cell sheets, tubes and vesicles. Heterogeneous cell populations may preferentially either intermix or sort out, depending upon the balance of adhesive forces between like and unlike elements. The precise configuration adopted will depend upon the particular adhesive relationships that prevail. Both this end state and the approach toward it arise from the adhesive relationships among the interacting cells. Such morphogenetic phenomena as tissue spreading and the segregation of organ primordia are probably brought about in this way. We outline here some results of our recent experiments on the morphogenesis of the salamander pronephric duct. These illustrate the reality of emergent adhesion-generated tissue immiscibility as a cause of organ segregation and point toward a craniocaudally travelling adhesion gradient as the information that guides the migrating pronephric duct to the cloaca.

Ambystoma↗
PubMed2006

Microleakage beneath ceramic and metal brackets bonded with a conventional and an antibacterial adhesive system.

OBJECTIVE: To assess microleakage of a tooth-adhesive-bracket complex when metal or ceramic brackets were bonded with a conventional and an antibacterial self-etching adhesive. MATERIALS AND METHODS: Forty freshly extracted human premolars were randomly assigned to four equal groups and received the following treatments: group 1 = Transbond XT + metal bracket, group 2 = Transbond XT + ceramic bracket, group 3 = Clearfil Protect Bond + ceramic bracket, and group 4 = Clearfil Protect Bond + metal bracket. After photopolymerization, the teeth were kept in distilled water for 1 month and thereafter subjected to thermal cycling (500 cycles). Specimens were further sealed with nail varnish, stained with 0.5% basic fuchsin for 24 hours, sectioned and examined under a stereomicroscope, and scored for marginal microleakage for the adhesive-tooth and bracket-adhesive interfaces from incisal and gingival margins. Statistical analysis was accomplished by Kruskal-Wallis test and Mann-Whitney U-test with Bonferroni correction. RESULTS: All groups demonstrated microleakage between the adhesive-enamel and bracket-adhesive interfaces. A significant difference was observed among all groups (P < .05) for the microleakage between the bracket-adhesive interface. Metal brackets exhibited significantly more microleakage than did ceramic brackets between the bracket-adhesive interface with either of the adhesives. Clearfil Protect Bond exhibited results similar to Transbond XT. Clearfil Protect Bond may be a choice of adhesive in bracket bonding because of its antibacterial activity and similar microleakage results with the orthodontic adhesive. CONCLUSIONS: Metal brackets cause more leakage between an adhesive-bracket interface, which may lead to lower clinical shear bond strength and white-spot lesions.

Bicuspid↗
PubMed1999

Influence of the time-point of salivary contamination on dentin shear bond strength of 3 dentin adhesive systems.

PURPOSE: The aim of this study was to evaluate the influence of the duration of salivary contamination at different stages during the bonding procedures on shear bond strengths (SBS) of 3 dentin adhesives. MATERIALS AND METHODS: Flat human dentin surfaces were produced by wet grinding on SiC paper 800. The adhesives used were Syntac Sprint (SS) (Vivadent), One Step (OS) (Bisco), Clearfil Liner Bond 2 (LB2) (Kuraray). Three durations of contamination (3 s, 10 s, and 20 s) at 3 stages (before adhesive application, after its application, and after its polymerization). In all cases the saliva was not rinsed off. Twenty-seven groups of 10 samples were studied according to 3 adhesives, 3 stages, and 3 durations of contamination. For each adhesive, 1 control group, 3 groups with contamination before adhesive application, 3 groups with salivary contamination on the uncured adhesive, and 3 groups with contamination after polymerization (except for SS) were studied. Composite cylinders (Z100, 3M; 3 mm Ø, 5 mm high) were polymerized on the surfaces and stored in 37 degrees C H2O for 48 hours prior to shear bond testing (v = 5 mm/min). RESULTS: Anova and Scheffe tests showed that for the one-bottle systems tested, salivary contamination prior to adhesive application had no adverse effect on bonding efficacy, SBS decreased significantly when saliva contamination occurred after adhesive application. The self-etching primer tested was more tolerant to salivary contamination, except when the salivary contamination occurred before the polymerization of the adhesive. CONCLUSIONS: Salivary contamination does not have the same influence at different stages of the bonding process with modern adhesives. Pending better knowledge of the mechanisms involved in the influence of salivary contamination on bonded assemblies, it seems necessary to continue to recommend using the rubber dam in adhesive dentistry.

Acrylates↗
PubMed1996

The relationships among adhesion, stratification and differentiation in keratinocytes.

Epidermis is a self-renewing, multilayered tissue composed primarily of keratinocytes. The epidermal keratinocyte follows a terminal differentiation pathway that under normal circumstances is tightly linked to its position within the epidermis and culminates in the formation of the protective barrier (stratum corneum) that constitutes the outermost layer of skin. Strong but pliant adhesive mechanisms are essential for normal functioning of the epidermis. In the epidermis, adhesion is mediated primarily by four structures: hemidesmosomes and focal adhesions, which function in cell-matrix adhesion, and desmosomes and adherens junctions, which function in cell-cell adhesion. In this review we concentrate on the transmembrane components of these structures, which are thought to mediate directly the adhesive function. Members of the integrin family of adhesion molecules comprise the transmembrane components of hemidesmosomes and focal adhesions, although hemidesmosomes also have a second, unrelated transmembrane molecule known as 'bullous pemphigoid antigen 2'. Members of the cadherin family are the transmembrane constituents of desmosomes and adherens junctions. Desmosomes consistently contain two types of cadherins (desmoglein and desmocollin), while adherens junctions may contain only one type of cadherin (E- or P-cadherin). Expression of most of the transmembrane components varies with the position of the keratinocyte within the epidermis and thus may reflect the degree of epidermal differentiation. All of the integrin subunits have been localized predominantly to the basal layer. In contrast, the cadherins show very complex expression patterns throughout the epidermis. Desmogleins and desmocollins (the desmosomal cadherins) are each encoded by three genes, and the expression of each gene is limited to certain epidermal layers. With respect to the cadherins of the adherens junction, it has been shown that E-cadherin is present throughout the epidermis, while P-cadherin is limited to the basal layer. Interestingly, these complex expression patterns of integrins and cadherins within the epidermis may not simply be passive events in differentiation; rather, evidence is accumulating that adhesion molecules can exert a dynamic role in epidermal differentiation/stratification. For example, decreased adhesion to extracellular matrix, induced by changes in one or more integrins, appears to be a signal that induces certain differentiation-related events. Even more profound effects on epidermal morphogenesis have been demonstrated for the cadherins. E- and/or P-cadherin is required not only to initiate normal intercellular junction formation but also for the subsequent development of a stratified epithelium. Thus, the findings to date with both integrins and cadherins suggest that adhesion molecules may function not just as direct mediators of adhesion, but also as regulators of epidermal stratification, differentiation, and morphogenesis.

Journal Article↗
PubMed1996

Salicylates inhibit I kappa B-alpha phosphorylation, endothelial-leukocyte adhesion molecule expression, and neutrophil transmigration.

The expression of leukocyte adhesion molecules on endothelial cells is induced by TNF-alpha and other inflammatory cytokines. This induction of endothelial-leukocyte adhesion molecule-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 requires the transcription factor nuclear factor-kappa B (NF-kappa B). Recent work has suggested that some nonsteroidal anti-inflammatory agents, including sodium salicylate and aspirin, can inhibit NF-kappa B-dependent gene activation. We studied the effects of salicylates on expression of adhesion molecules in HUVECs. We found that sodium salicylate inhibited activation of NF-kappa B (p50/p65 and p65/p65) by preventing phosphorylation and subsequent degradation of the inhibitor 1 kappa B-alpha. Salicylate treatment had no effect on TNF-alpha-induced phosphorylation of the transcription factor ATF-2. Salicylate blocked the TNF-alpha-induced increase in mRNA levels of adhesion molecules and gave a dose-dependent inhibition of TNF-alpha-induced surface expression of vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 with higher doses required to inhibit endothelial-leukocyte adhesion molecule-1 expression. Indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expression of adhesion molecules, suggesting that the effects were not due to inhibition of cyclooxygenase. Treatment of endothelial cell monolayers with sodium salicylate inhibited transendothelial migration of neutrophils but had no significant effect on neutrophil adhesion under flow conditions. The clinical importance of high-dose salicylates in inflammation may be due, in part, to the ability to prevent expression of inducible adhesion molecules and recruitment of leukocytes.

Base Sequence↗
PubMed1997

Bond strengths of the adhesive resin-amalgam interface.

PURPOSE: To evaluate the tensile and shear bond strengths of eight adhesives and two amalgams (spherical and lathe cut). MATERIALS AND METHODS: Two high-copper amalgams (Tytin, spherical; and ANA-2000, dispersed phase) and seven adhesives (Panavia EX, C&B Metabond, Chameleon Metal Resin Cement, All-Bond 2, All-Bond C&B, Photo-Bond and Imperva Dual) were evaluated. An epoxy resin (Stycast 1266) was included as a control for comparison because it was an adhesive material of similar viscosity but different chemistry from the dental adhesives. The aluminum surfaces were sandblasted with 50 microns aluminum oxide just prior to coating with adhesive resins. The testing area was defined with a 4 mm circular adhesive Mylar mask. All adhesives were mixed and handled according to manufacturers' instructions. Freshly mixed amalgam was condensed into the test cavity and onto the surface immediately after coating with adhesive. After 24 hours storage, the bond strengths were determined in an Instron testing machine at a crosshead speed of 2 mm/minute. The debonded surfaces were examined in an optical microscope for site of failure. The few samples which showed failure at the aluminum-resin interface were not included in the study. Selected debonded surfaces were examined by SEM. A 2-way ANOVA (General Levin Models-GLM) was used to analyze the data from both the tensile and shear bond strength tests. GLM was used instead of standard ANOVA because of the unbalanced design. The lack of balance occurred because some of the bonding resin/amalgam groups had different sample numbers. RESULTS: A wide variation in bond strengths was obtained with adhesive resin cements and not all appeared suitable for adhesive amalgam restorations. Panavia EX, C&B Metabond, Chameleon Metal Resin Cement and All-Bond C&B showed the best potential for amalgam bonding, with shear and tensile bond strengths greater than 8 MPa. Viscous, filled versions of adhesives appeared to be more effective. Choice of amalgam appeared to be less important than choice of adhesive.

Analysis of Variance↗
PubMed1992

A method to determine shear adhesive strength of fibrin sealants.

The adhesive strength of fibrin sealants has not been rigorously evaluated to date. The adhesive strength of six different concentrations of cryoprecipitated fibrinogen as well as the commercially available fibrin tissue adhesive Tissucol was tested under controlled conditions utilizing split-thickness skin grafts as the test adherand. This test configuration permitted the modeling of bonding strength for attachment of skin grafts as well as incorporate established engineering test standards for adhesives. An increase in fibrin concentration corresponded with an increase in shear adhesive strength. No significant increases in adhesive strength were attained after 5 min of bonding for all tested concentrations, except for the commercial adhesive, which attained the adhesive strength of an equivalent concentration of cryoprecipitated adhesive after 90 min. The adhesive strength, however, was an order of magnitude less than reported values of the tensile strength of fibrin material for similar concentrations. Therefore, it is important that the surgeon use a sufficiently high fibrinogen concentration for the specific clinical indication. The method of fibrin sealant preparation and/or the compounding adjuncts appear to have an effect on the development of adhesive strength.

Adhesiveness↗
PubMed2001

Adhesion of epithelial cells to fibronectin or collagen I induces alterations in gene expression via a protein kinase C-dependent mechanism.

Adhesion of human salivary gland (HSG) epithelial cells to fibronectin- or collagen I gel-coated substrates, mediated by beta1 integrins, has been shown to upregulate the expression of more than 30 genes within 3-6 h. Adhesion of HSG cells to fibronectin or collagen I for 6 h also enhanced total protein kinase C (PKC) activity by 1.8-2.3-fold. HSG cells expressed PKC-alpha, gamma, delta, epsilon, mu, and zeta. Adhesion of HSG cells to fibronectin or collagen I specifically activated PKC-gamma and PKC-delta. Cytoplasmic PKC-gamma and PKC-delta became membrane-associated, and immunoprecipitated PKC-gamma and PKC-delta kinase activities were enhanced 2.5-4.0-fold in HSG cells adherent to fibronectin or collagen I. In addition, adhesion of fibronectin-coated beads to HSG monolayers co-aggregated beta1 integrin and PKC-gamma and PKC-delta but not other PKC isoforms. Thus, integrin-dependent adhesion of HSG cells to fibronectin or collagen I activated PKC-gamma and PKC-delta. The role of this PKC upregulation on adhesion-responsive gene expression was then tested. HSG cells were treated with the specific PKC inhibitor bisindolylmaleimide I, cultured on non-precoated, fibronectin- or collagen I-coated substrates, and analyzed for changes in adhesion-responsive gene expression. Bisindolylmaleimide I strongly inhibited the expression of seven adhesion-responsive genes including calnexin, decorin, S-adenosylmethionine decarboxylase, steroid sulfatase, and 3 mitochondrial genes. However, the expression of two adhesion-responsive genes was not affected by bisindolylmaleimide I. Treatment with bisindolylmaleimide I did not affect cell spreading and did not significantly affect the actin cytoskeleton. These data suggest that adhesion of HSG cells to fibronectin or collagen I induces PKC activity and that this induction contributes to the upregulation of a variety of adhesion-responsive genes.

Cell Adhesion↗
PubMed1997

Pervanadate-induced adhesion of CD4+ T cell to fibronectin is associated with tyrosine phosphorylation of paxillin.

The initial stages of T cell activation involve tyrosine protein kinase-mediated intracellular signaling events. Integrin-mediated adhesion of CD4+ T lymphocytes to extracellular matrix glycoproteins, such as fibronectin, is an activation-dependent process. The involvement of tyrosine protein kinases in the adhesion of CD4+ T cells to fibronectin was examined using pervanadate, a protein-tyrosine phosphatase inhibitor. Pervanadate induced the adhesion of human CD4+ T cells to immobilized fibronectin in a beta1 integrin-mediated fashion, and adhesion was associated with an increase of protein tyrosine phosphorylation. Tyrosine protein kinase inhibitors abrogated both T cell adhesion and intracellular protein tyrosine phosphorylation. Participation of cytoskeletal proteins in the pervanadate-induced T cell adhesion was indicated because cytoskeleton disruption by cytochalasin B inhibited cell adhesion to fibronectin. We demonstrate that the cytoskeletal protein paxillin underwent time-dependent tyrosine phosphorylation simultaneously with pervanadate-induced T cell adhesion to fibronectin. Tyrosine phosphorylation of paxillin was related to cell adhesion, since pretreatment of T cells with cytochalasin B abrogated both adhesion and phosphorylation. This study demonstrates a correlation between activation of protein tyrosine kinases, tyrosine phosphorylation of paxillin, and integrin-mediated T cell adhesion to extracellular matrix glycoproteins.

CD4-Positive T-Lymphocytes↗
PubMed1998

Mode of adsorption and orientation of an extracellular matrix protein affect its cell-adhesion-promoting activity.

Cell adhesion to extracellular matrix contributes to the organization of tissues and modulates cell behavior. In conventional cell adhesion assays, plastic wells are coated with matrix proteins and assayed for their adhesion-promoting activity. We show here that factors such as sample composition, coating buffers, and manufacturers' plastic treatment markedly affect cell adhesion to the extracellular matrix protein laminin-5 (Ln-5). These factors were shown to affect adsorption efficiency as determined by measuring total adsorbed protein with a polyclonal anti-Ln-5 antiserum. They also influence the availability of the epitope for an adhesion-blocking anti-Ln-5 monoclonal antibody, suggesting that coating conditions affect the orientation of Ln-5. Generally, cell adhesion correlates more strongly with the availability of the epitope for the adhesion-blocking antibody than with total adsorbed Ln-5. Our data further indicate that cell adhesion to other matrix proteins may be influenced by similar factors. Adding Ln-5 samples to plastic wells that had been precoated with non-adhesion-blocking anti-Ln-5 antibodies made cell adhesion independent of factors such as sample composition, coating buffers, and source of plastic. Thus, the control of adsorption efficiency and orientation of extracellular matrix proteins is essential for creation of reliable and reproducible conditions in cell adhesion assays.

Adsorption↗
PubMed1996

Carbohydrate- and CD18-dependent neutrophil adhesion to cardiac myocytes: effects of adenosine.

OBJECTIVE: Adenosine inhibits neutrophil adhesion and injury to isolated cardiac myocytes. In the present study, the contribution of selectin and CD18 interactions to neutrophil-myocyte adhesion and their sensitivity to adenosine were assessed. METHODS: Activated human neutrophils and canine myocytes were incubated with inhibitors of CD18 or selectin binding, adenosine, or combinations of both for 30-50 min at 37 degrees C. Neutrophils were pretreated with 0.1 microM fMLP for 10 min to study L-selectin-independent adhesion. Adhesion was measured by phase contrast microscopy. RESULTS: Anti-L-selectin mAb and the selectin-blocking carbohydrates sialyl Lewisx or mannose-6-phosphate, as well as anti-CD18 or anti-ICAM-1 mAbs, inhibited cell adhesion (by 84-99%, P < 0.05). CD11a, but not CD11b, was responsible for most of the CD18-mediated binding. An L-selectin-independent interaction between neutrophils and cardiac myocytes was observed that was delayed (peak adhesion at 40-50 min, rather than 30 min), but still inhibited by anti-CD18 mAb (by 65 +/- 11%, P < 0.05) and carbohydrates (by 87-97%, each P < 0.05). Adenosine (100 nM) inhibited this late CD18-dependent/L-selectin-independent phase of adhesion (by 61 +/- 14%, P < 0.05). The combination of adenosine and anti-CD18 mAb was additive such that adhesion was completely blocked (P < 0.05, compared to either agent alone). Inhibition of adhesion by adenosine was prevented by the A2 antagonist, DMPX (100 nM), and mimicked by the A2 agonist, CGS-21680 (10 nM) or the adenosine regulating agents, acadesine (100 microM) or GP531 (10 microM). CONCLUSION: Neutrophil-myocyte adhesion involved both L-selectin-dependent and L-selectin-independent carbohydrate binding as well as CD11a/CD18. Inhibition of adhesion by adenosine interferes with L-selectin-independent carbohydrate binding and possibly CD18.

Adenosine↗
PubMed1992

Differential adhesion of granulocytes to five distinct phenotypes of cultured microvascular endothelial cells.

Adhesion of isolated human polymorphonuclear granulocytes (PMNs) to five different phenotypes of cultured microvascular endothelial cells derived from bovine corpora lutea was investigated by measuring the myeloperoxidase content of cell lysates. Untreated and interleukin 1 (IL-1) -pretreated confluent monolayers were overlaid with unstimulated and phorbol ester (PMA)-stimulated PMNs in the absence and presence of the monoclonal antibody IB4 recognizing and functionally blocking beta 2 (CD18) of the leukocyte integrins. Unstimulated PMN adhesion was highest on type 4, followed by type 3 and 5 endothelial cells. This adhesion was not inhibited by treatment with IB4. IL-1 pretreatment of endothelial cells resulted in a significant increase of PMN adhesion on types 1, 2, and 4, most of which was also beta 2 integrin-independent. PMA-stimulation of PMNs increased adhesion to maximal values on cell types 1 and 5, which was largely blocked by IB4. Type 2 endothelial cells supported significantly less PMA-stimulated PMN adhesion than all other types. In the presence of IB4, adhesion of PMNs to untreated and IL-1-pretreated type 3 and 4 endothelial cells was significantly reduced by PMA. This reduction of beta 2 integrin-independent adhesion by PMA stimulation is compatible with possible shedding of the lectin-like leukocyte adhesion molecule, L-selectin, from PMNs. Differential PMN adhesion may reflect distinctive expression of endothelial adhesion molecules in different phenotypes of microvascular endothelial cells. Endothelial specialization within the microcirculation may have important functional consequences for the inflammatory response in vivo.

Animals↗
PubMed1990

Leucocyte cellular adhesion molecules.

Leucocytes express adhesion promoting receptors which mediate cell-cell and cell-matrix interactions. These adhesive interactions are crucial to the regulation of haemopoiesis and thymocyte maturation, the direction and control of leucocyte traffic and migration through tissues, and in the development of immune and non-immune inflammatory responses. Several families of adhesion receptors have been identified (Table). The leucocyte integrin family comprises 3 alpha beta heterodimeric membrane glycoproteins which share a common beta subunit, designated CD18. The alpha subunits of each of the 3 members, lymphocyte function associated antigen-1 (LFA-1), macrophage antigen-1 (Mac-1) and p150,95 are designated CD11a, b and c respectively. These adhesion molecules play a critical part in the immune and inflammatory responses of leucocytes. The leucocyte integrin family is, in turn, part of the integrin superfamily, members of which are evolutionally, structurally and functionally related. Another Integrin subfamily found on leucocytes is the VLA group, so-called because the 'very late activation antigens' VLA-1 and VLA-2 were originally found to appear late in T-cell activation. Members of this family function mainly as extracellular matrix adhesion receptors and are found both on haemopoietic and non-haemopoietic cells. They play a part in diverse cellular functions including tissue organisation, lymphocyte recirculation and T-cell immune responses. A third integrin subfamily, the cytoadhesins, are receptors on platelets and endothelial cells which bind extracellular matrix proteins. A second family of adhesion receptors is the immunoglobulin superfamily, members of which include CD2, LFA-3 and ICAM-1, which participate in T-cell adhesive interactions, and the antigen-specific receptors of T and B cells, CD4, CD8 and the MHC Class I and II molecules. A recently recognised family of adhesion receptors is the selectins, characterised by a common lectin domain. Leucocyte adhesion molecule-1 (LAM-1), which is the human homologue of the murine homing receptor, MEL-14, is expressed on leucocytes, while endothelial leucocyte adhesion molecule-1 (ELAM-1) and granule membrane protein (GMP-140) are expressed on stimulated endothelial cells and activated platelets. This review will be confined to adhesion receptors found on leucocytes, with particular emphasis on the leucocyte integrins.

Animals↗
PubMed1994

The relative roles of vitronectin receptor, E-selectin and alpha 4 beta 1 in cancer cell adhesion to interleukin-1-treated endothelial cells.

Adhesion of cancer cells to endothelium is thought to be a prerequisite to extravasation during the haematogenous phase of metastasis, and is enhanced after perturbation of the endothelium by interleukin-1 (IL-1). The inducible endothelial adhesion molecules, E-selectin, VCAM-1/alpha 4 beta 1 and vitronectin receptor have been reported to mediate attachment of cancer cells to IL-1-treated endothelial cells. We have examined the relative contribution of these molecules by quantifying the adhesion of a panel of 22 human, 125I-labelled cancer cells and the rat W256 tumour to untreated and IL-1-treated endothelial monolayers in the presence of relevant neutralising antibodies. Antibodies against E-selectin inhibited the adhesion of HL-60 leukaemia cells and two colon carcinomas. Anti-alpha 4 beta 1 antibodies blocked adhesion of four melanomas, five sarcomas and one lung carcinoma. Anti-vitronectin receptor antibodies inhibited adhesion of 14 of the 22 human cell lines to IL-1-treated endothelial cells. Adhesion of seven cell lines was inhibited by more than a single antibody. In contrast, adhesion of one of the cancer cell lines was unaffected by any of the antibodies, suggesting involvement of other IL-1-inducible endothelial adhesion molecules. Moreover, none of the antibodies altered the attachment of cancer cells to unstimulated endothelial monolayers. We conclude that the mechanisms of cancer cell adhesion to the endothelium are influenced by endothelial activation and by the adhesive repertoire of the cancer cell.

Animals↗
PubMed2005

Control of focal adhesion dynamics by material surface characteristics.

The mechanisms of cell adhesion to the extracellular matrix (ECM) which are of fundamental importance for function, survival, and growth of cells involve the formation of focal adhesions to facilitate integrin signaling. Recently, it became evident that focal adhesions are not stable but move to enable cell migration and ECM formation. We examined the number, size, and dynamic behavior of focal adhesions in living MG-63 osteoblastic cells, which were cultured on titanium surfaces with different roughnesses and on stainless steel (SS). As a marker for focal adhesions we used GFP-tagged vinculin, a cytoskeletal protein. Focal adhesions were smaller on titanium and on SS than on collagen-coated glass coverslips. The corundum-blasted rough surface of titanium induced the smallest adhesions. On all the surfaces that we have tested, we observed a mobility of focal adhesions. On collagen-coated coverslips focal adhesions moved with a speed of 60 nm/min. The speed was reduced on titanium and still more restricted on SS. The topography did not affect the mobility of focal adhesions. We conclude that on the material surfaces that we have studied a reduced mobility of focal adhesions may strengthen the linkages between cell and ECM but impair the ability to dynamically organize and remodel the ECM. The results may have a great impact in the functional evaluation of tailored biomaterial surfaces for the application in tissue engineering.

Biocompatible Materials↗
PubMed1997

Parturition: steroids, prostaglandin E2, and expression of adhesion molecules by endothelial cells.

OBJECTIVE: To determine whether 17 beta-estradiol, progesterone, and prostaglandin (PG) E2, alone or in combination with cytokines, influence the adhesiveness of vascular endothelium and thus play a role in the first stage of leukocyte infiltration of the uterine cervix during parturition. METHODS: Cultured umbilical vein endothelial cells obtained from 11 women after vaginal delivery at term were incubated with 17 beta-estradiol, progesterone, PGE2, tumor necrosis factor alpha (TNF-alpha), and interleukin-8, (IL-8), alone and in combination. The expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 was investigated by immunofluorescence and flow cytometry. The Kolmogorov-Smirnov test was used for statistical analysis. RESULTS: We found that 17 beta-estradiol augmented the TNF-alpha-induced expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 by 107, 9, and 39%, respectively. Alone, 17 beta-estradiol induced the expression of only intercellular adhesion molecule-1 (24%), as did PGE2 (13%). Neither progesterone nor IL-8 induced expression of any of these adhesion molecules. CONCLUSIONS: Unlike progesterone, 17 beta-estradiol and PGE2 stimulate the expression of adhesion molecules in vitro and may, therefore, promote adhesion of granulocytes to capillary endothelium.

Cells, Cultured↗