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Results for “Cell Adhesion”

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PubMed1995

Increased adhesion to vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 of eosinophils from patients with asthma.

Adhesion of peripheral blood eosinophil and neutrophil granulocytes to the endothelial cell adherence receptors E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 has been measured. The study included patients with allergic rhinitis, patients with mild allergic and nonallergic asthma, and healthy individuals; 10 persons were in each group. In addition, assay of eosinophil and neutrophil cell surface expression of the receptor complex CD11b/CD18 was performed. Increased eosinophil adhesion to vascular cell adhesion molecule-1 (p < 0.05) and intercellular adhesion molecule-1 (p < 0.05) was demonstrated in the patients with a more labile asthma, that is, a peak expiratory flow rate variability of more than 10%, suggesting a relationship to the degree of ongoing inflammation in the airways of the patients. The increased eosinophil adhesion was most probably due to a functional upregulation of the CD11b/CD18 and very late activation antigen-4 receptors, because the number of receptors measured as cell surface expression was unaltered. The increased eosinophil adhesion in the patients with high peak expiratory flow rate variability appeared independent of atopy. The increased adhesion was not entirely specific to the eosinophils, because neutrophils from patients with a peak expiratory flow rate variability of more than 10% also demonstrated increased adhesion to intercellular adhesion molecule-1 (p < 0.05) when compared with neutrophils from the patients with low peak expiratory flow rate variability. In conclusion, the demonstrated priming of eosinophil adhesion to vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 might be one contributing mechanism behind the selective accumulation of eosinophils in the lung tissue of patients with asthma.

Adult↗

PubMed1997

Molecular interactions in cell adhesion complexes.

Cell adhesions consist of multimolecular protein complexes of transmembrane adhesion receptors anchoring intracellular cytoskeletal structural proteins and signal transduction molecules. Recent advances reveal that components of cell adhesion complexes display multiple interactions and functions, which cooperate to mediate both cell adhesion and signaling. Cell-matrix and cell-cell adhesions can serve as both recipients and generators of signaling information, using hierarchical and synergistic molecular interactions regulated by aggregation, conformational changes, phosphorylation, and tension.

Cell Adhesion↗

PubMed2004

Elevated soluble cell adhesion molecules E-selectin and intercellular cell adhesion molecule-1 in type-2 diabetic patients with and without asymptomatic peripheral arterial disease.

AIM: Cell adhesion molecules may serve as markers of endothelial cell activation, and they may well have a role in the pathogenesis of atherosclerotic vascular disease in diabetes mellitus. METHODS EXPERIMENTAL DESIGN: a cross sectional, comparative study. SETTING: a teaching University Hospital. Patients and controls. A cohort of diabetic patients with absent peripheral arterial pulses but no history of cardiovascular or cerebrovascular disease i.e. asymptomatic (n=29), median age 68 (36-80) years, (range), diabetes duration 10 (1-43) years and HbA1c 7.7% (4.8-9.6). They were compared to 12 age and sex matched normal non-diabetic controls. INTERVENTION: none. MEASURES: soluble cell adhesion molecules intercellular cell adhesion molecule-1 (ICAM-1) and E-selectin levels measured by ELISA methods. RESULTS: The 29 patients with diabetes, as a whole, were found to have significantly higher median plasma sICAM-1 and sE-selectin of 283 ng/ml (154-1000) (range), and 65.8 ng/ml (20.6-145) vs 237 (147-312.4) and 37.7 (19.8-46.6) respectively, Mann Whitney U test p<0.02, and p<0.002. In the diabetic group, E-selectin correlated with ICAM-1, age and HbA1c: r=0.524 p<0.01, r=0.385 p<0.05 and r=0.393 p<0.05 respectively (Spearman correlation coefficient). CONCLUSION: These results confirm that elevated levels of adhesion molecules, E-selectin and ICAM-1 occur in Type-2 diabetes early in the course of asymptomatic peripheral arterial occlusive disease, and this is related to glycemic control. This suggests that adhesion molecules may have a role in the pathogenesis of atherosclerotic vascular disease in diabetes.

Adult↗

PubMed1994

Distinct but overlapping epitopes are involved in alpha 4 beta 7-mediated adhesion to vascular cell adhesion molecule-1, mucosal addressin-1, fibronectin, and lymphocyte aggregation.

The mouse CD8+ T cell lymphoma TK1 expresses high levels of alpha 4 beta 7 integrin, which it can use to interact with multiple ligands including mucosal addressin-1 (MAdCAM-1), VCAM-1, and fibronectin. In addition, alpha 4 beta 7 can support TK1 cell aggregation. Here we have produced and characterized a panel of mAbs against alpha 4 beta 7 to define antigenic and functional epitopes associated with its distinct functions. One mAb, DATK32, is unique in recognizing an epitope specific to the alpha 4 beta 7 heterodimer. Furthermore, DATK32 induces TK1 cell aggregation yet inhibits TK1 cell adhesion to MAdCAM-1, VCAM-1, and fibronectin. Considered as a whole, the panel of anti-alpha 4 beta 7 mAbs studied define unique patterns of inhibition for alpha 4 beta 7 binding to each of its defined molecular ligands. We conclude that alpha 4 beta 7 interactions with MAdCAM-1, VCAM-1, and fibronectin can be modulated by Ab binding to distinct epitopes and thus probably involve functionally separable, although physically overlapping binding sites on this multifunctional integrin. These findings are consistent with the general observation that integrins use distinct, potentially differentially regulated interaction sites for adhesion to multiple ligands. Extension of these concepts to alpha 4 beta 7 has important considerations for understanding the roles of this integrin in lymphocyte homing to mucosal sites and in cell-cell interactions during the immune response.

Animals↗

PubMed1991

Four molecular pathways of T cell adhesion to endothelial cells: roles of LFA-1, VCAM-1, and ELAM-1 and changes in pathway hierarchy under different activation conditions.

T cell adhesion to endothelium is critical to lymphocyte recirculation and influx into sites of inflammation. We have systematically analyzed the role of four receptor/ligand interactions that mediate adhesion of peripheral human CD4+ T cells to cultured human umbilical vein endothelial cells (HUVEC): T cell LFA-1 binding to ICAM-1 and an alternative ligand ("ICAM-X"), T cell VLA-4 binding to VCAM-1, and T cell binding to ELAM-1. Contributions of these four pathways depend on the activation state of both the T cell and HUVEC, and the differentiation state of the T cell. ELAM-1 plays a significant role in mediating adhesion of resting CD4+ T cells to activated HUVEC. LFA-1 adhesion dominates with PMA-activated T cells but the strength and predominant LFA-1 ligand is determined by the activation state of the HUVEC; while ICAM-1 is the dominant ligand on IL-1-induced HUVEC, "ICAM-X" dominates binding to uninduced HUVEC. Adhesion via VLA-4 depends on induction of its ligand VCAM-1 on activated HUVEC; PMA activation of T cells augments VLA-4-mediated adhesion, both in the model of T/HUVEC binding and in a simplified model of T cell adhesion to VCAM-1-transfected L cells. Unlike LFA-1 and VLA-4, ELAM-1-mediated adhesion is not increased by T cell activation. Differential expression of adhesion molecules on CD4+ T cell subsets understood to be naive and memory cells also regulates T/HUVEC adhesion. Naive T cell adhesion to HUVEC is mediated predominantly by LFA-1 with little or no involvement of the VLA-4 and ELAM-1 pathways. In contrast, memory T cells bind better to HUVEC and utilize all four pathways. These studies demonstrate that there are at least four molecular pathways mediating T/HUVEC adhesion and that the dominance/hierarchy of these pathways varies dramatically with the activation state of the interacting cells and the differentiation state of the T cell.

Animals↗

PubMed2001

Relationship between the increase of secretion of sTNF alpha induced by lipopolysaccharides and the enhanced expression of TACE mRNA in HL-60 cells and adhesive cells from human spleen.

In order to find out the potential modulators which influence the secretion of TNF alpha, the relationship between the amount of secreted TNF alpha (sTNF alpha) and the level of TNF alpha converting enzyme (TACE) gene expression was studied before and after the stimulation by lipopolysaccharides (LPS) to HL-60 cells and adhered cells isolated from human spleen using cytological and molecular biology techniques and methods (RT-PCR, Dot-blot hybridization, etc.). The experimental results showed that: (1) LPS could induce the increase of expression of TNF alpha mRNA and TACE mRNA, reaching the peak value at 6 h and 10 h respectively after addition of LPS into cell culture medium; (2) The anti-sense oligodeoxyribonucleotide (A-ODN) complementary to TACE mRNA sequence really inhibited the secretion of TNF alpha as a result of blocked translation of TACE gene; (3) Furthermore, it was also observed that RDQ, a kind of injection derived from Chinese traditional herb, had strongly inhibitory effects on the expression of TACE mRNA and secretion of sTNF alpha stimulated by LPS. The above results suggested that the TACE indeed involved in delivering and processing of pro-TNF alpha during the period of LPS stimulation and the study about the regulator/inhibitors of TACE gene expression would be very important to develop new types of therapy agents against toxic and side effects of sTNF alpha during the period of infection/inflammation to human body.

ADAM Proteins↗

PubMed1998

Functional cooperation of cyclin C and c-Myc in mediating homotypic cell adhesion via very late antigen-4 activation and vascular cell adhesion molecule-1 induction.

Very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1) are a pair of adhesion molecules mediating cell-cell interaction. The binding activity of each depends on its surface expression, yet integrin activity can also be modulated through inside-out signaling. However, the specific intracellular molecules involved in modulating integrin VLA-4 activation via inside-out signaling or in regulating VCAM-1 expression are poorly understood. We show here that constitutive coexpression of cyclin C and c-Myc in hematopoietic BAF-B03 cells induces homotypic cell adhesion, which results from enhanced VLA-4 ligand-binding activity and induced expression of VCAM-1. Furthermore, regulation of cell adhesion appears to be a feature unique to cyclin C, but not other G1 cyclins, E and D3, and its regulatory function is independent of CDK8 kinase activity. Our results provide a novel role for cyclin C and c-Myc in the regulation of cell adhesion through distinct mechanisms.

Animals↗

PubMed2002

The effects of a protease inhibitor fraction from tepary bean (Phaseolus acutifolius) on in vitro cell proliferation and cell adhesion of transformed cells.

Some protease inhibitors (PI), such as the soybean Bowman-Birk protease inhibitor (SBBI), have been described as anticarcinogenic agents. Although PI are ubiquitous compounds in living organisms, the anticarcinogenic potential of PIs other than SBBI remain poorly explored. We evaluated the antiproliferative effect of a protein fraction from tepary bean (Phaseolus acutifolius) seeds with protease inhibitor activity (TPIF), on normal and on malignant cells. TPIF was obtained after precipitation with ammonium sulfate and gel filtration, and its bioactivity was assayed in vitro on HeLa cells, normal 3T3 fibroblasts and 3T3/v-mos transformed fibroblasts. TPIF showed antiproliferative and cytotoxic effects on 3T3/v-mos transformed fibroblasts in a dose-dependent way. On the contrary, TPIF was only cytostatic for normal 3T3 cells at the highest doses assayed, and had no effect on epithelial HeLa cells proliferation. Sublethal TPIF doses also stimulated cell adhesion of poorly adherent 3T3/v-mos cell line.

3T3 Cells↗

PubMed2006

Addressing the role of cell adhesion in tumor cell dormancy.

The dissemination of tumor cells prior to the surgical resection of early stage tumors poses a serious risk to the disease free survival of cancer patients. This risk arises from the latent capacity of these cells to form solid metastatic lesions after a prolonged period of dormancy, exacerbated by the fact that these cells are often refractory to adjuvant chemotherapeutic protocols. Ensuring the long term survival of cancer patients therefore necessitates an understanding of the mechanisms of tumor cell dormancy and the accompanying drug resistance. Experiments designed to compare the biological behavior of metastatic versus nonmetastatic variants of tumor cells provide evidence that there exists a phenomenon of single-cell dormancy which may depend on a reciprocal dialogue between the tumor cell and the tissue microenvironment. Through a combination of 3-dimensional cell culture technique and in vivo models investigators are now beginning to elucidate the molecular mechanisms underlying this phenomenon. Here we review the results of a series of experiments describing the role of cell adhesion events in dictating tumor cell behavior, including the balance between proliferation and dormancy, and the acquisition of drug resistance.

Animals↗

PubMed1993

Effect of cytokines on the expression of cell adhesion molecule and on the adhesion of melanoma cells to endothelial cells.

We examined the role of cell adhesion molecules (CAM) by which tumor cells bind to the endothelial cells using human umbilical vein endothelial cells (HUVEC) and cultured melanoma cells. Endothelial cells from human umbilical veins were isolated and examined for CAM expression and its modulation by tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-6 (IL-6) or interferon-gamma (IFN-gamma). The expression of intercellular adhesion molecule 1 (ICAM-1) on HUVEC was increased by TNF-alpha, IL-1 and IFN-gamma when measured by ELISA or flow cytometric (FACS) analysis. IL-6 did not increase ICAM-1 expression on HUVEC. Two melanoma cell lines, Malme-3M and SK-Mel-28, showed increased expression of ICAM-1 after treatment with TNF-alpha, IL-1 and IFN-gamma in FACS analysis. IFN-gamma induced increased expression of HLA-DR only in SK-Mel-28 melanoma cells, not in Malme-3M melanoma cells. Neither HUVEC nor melanoma cells expressed lymphocyte function-associated antigen 1 (LFA-1) in either the basal (i.e., cytokine untreated) condition or the cytokine treated condition. Melanoma cells showed minimal increment in adhesion to TNF-alpha or IL-1 treated HUVEC than to cytokine untreated HUVEC. HUVEC and melanoma cells did not express LFA-1 and increased ICAM-1 expression by TNF-alpha, IL-1 and IFN-gamma treatment in FACS analysis did not coincide with minimal increase of melanoma cells adhesion to cytokine treated HUVEC. These results suggest that adhesion between melanoma cells and HUVEC is probably mediated by molecular interaction other than ICAM-1/LFA-1.

Cell Adhesion↗

PubMed1980

Analysis of the cell adhesion mechanism using somatic cell hybrids. I. Aggregation of hybrid cells between adhesive V79 and non-adhesive Ehrlich's ascites tumour cells.

V79 Chinese hamster cells dissociated with 1 nm EDTA retain 2 kinds of cell adhesion mechanisms, one dependent on Ca2+ and the other independent of Ca2+. Ehrlich's ascites tumour (EAT) cells are provided with neither Ca2+-dependent nor CA2+-independent mechanisms. Studies on the aggregation of cells of 25 different hybrid clones obtained by fusing these 2 lined cells revealed the following points with regard to adhesive properties of hybrid cells. (1) The activity of the Ca2+-independent mechanism was lower in most hybrid clones than in parental V79 cells. (2) There were a few hybrid clones whose Ca2+-dependent mechanism activity was lower than in V79 cells. In these clones, the Ca2+-independent mechanism was also less active than the parental cells. (3) A hybrid clone with reduced Ca2+-dependent mechanism activity only was not found. (4) All the hybrid clones have at least one set of chromosomes derived from V79. (5) The number of chromosomes derived from EAT cells tended to be less in hybrid clones with lower aggregative ability. These results can be explained by assuming that the activity of the Ca2+-independent and Ca2+-dependent mechanisms of V79 cells may be differently inhibited by genes contained in EAT cells.

Animals↗

PubMed2006

Human osteoblast-like cell adhesion on titanium substrates covalently functionalized with synthetic peptides.

Biomaterials to be used for the production of endosseous devices in dental, orthopedic and maxillo-facial applications, might be designed to support, guide and enhance osteoblast adhesion. Cell recruitment onto biomaterial surface is a fundamental step within the complex process responsible for implant osseointegration; this process involves several proteins from the extra cellular matrix (ECM), cytoskeleton and cell membrane. A new strategy to improve endosseous implant integration is based on preparing biomimetic surfaces able to present adhesive factors to cells. Osteoblast adhesion takes place by at least two different mechanisms: the most investigated one implies the interaction with RGD sequences via cell-membrane integrin receptors; a further mechanism concerns the interaction between cell-membrane heparan sulfate proteoglycans and heparin-binding sites of ECM proteins. In the present study two different biomimetic surfaces were obtained by covalently grafting two adhesive peptides on oxidized titanium substrates after silanization: an RGD-containing peptide and a peptide mapped on human vitronectin. The two sequences are known to act via different adhesive mechanisms. The amount of human osteoblasts adhered onto peptide-enriched or not enriched titanium oxidized surfaces and the strength of cell binding were estimated, thus comparing the capacity of the bioactive substrates in promoting cell adhesion.

Aged↗

PubMed2000

Nectin-3, a new member of immunoglobulin-like cell adhesion molecules that shows homophilic and heterophilic cell-cell adhesion activities.

We have isolated a novel cell-cell adhesion system localized at cadherin-based adherens junctions (AJs). This system consists of at least nectin, a Ca(2+)-independent immunoglobulin-like adhesion molecule, and afadin, an actin filament-binding protein, that connects nectin to the actin cytoskeleton. Nectin constitutes a family consisting of two members, nectin-1 and -2. We have isolated here a third member of the nectin family and named it nectin-3. Nectin-3 has three splicing variants, nectin-3alpha (biggest), -3beta (middle), and -3gamma (smallest). Like nectin-1 and -2, nectin-3alpha consists of three extracellular immunoglobulin-like domains, a transmembrane segment, and a cytoplasmic region with the C-terminal consensus motif for binding to the PDZ domain. Nectin-3alpha formed a cis-homo-dimer and showed Ca(2+)-independent trans-homo-interaction to cause homophilic cell-cell adhesion. Nectin-3alpha furthermore showed trans-hetero-interaction with nectin-1 or -2 but did not form a cis-hetero-dimer with nectin-1 or -2. Nectin-1 did not show trans-hetero-interaction with nectin-2. The affinity of trans-hetero-interaction of nectin-3alpha with nectin-1 or -2 was higher than that of trans-homo-interaction of nectin-1, -2, or -3alpha. Nectin-2 and -3 were ubiquitously expressed, whereas nectin-1 was abundantly expressed in brain. Nectin-3alpha was colocalized with nectin-2 at cadherin-based AJs and interacted with afadin. These results indicate that the nectin family consists of at least three members, nectin-1, -2, and -3, all of which show homophilic and heterophilic cell-cell adhesion activities and are localized at cadherin-based AJs.

Alternative Splicing↗

PubMed1986

Oligodendrocyte cell adhesion molecules are related to neural cell adhesion molecule (N-CAM).

The glycoproteins responsible for calcium-dependent oligodendrocyte aggregation were purified and characterized. Using detergent extraction, lentil-lectin-Sepharose 4B affinity chromatography, and preparative gel electrophoresis, 3 proteins were purified to apparent homogeneity, with relative Mrs of 120,000, 140,000, and 180,000. The aggregation assay showed that all 3 proteins had the ability to block antibody-mediated inhibition of oligodendrocyte aggregation. The 120,000 protein was the most active of the three. Antisera were raised in rabbits to these 3 individual proteins. Western blot analyses showed that all three antisera recognized 120,000, 140,000, and 180,000 proteins, which indicated that the proteins were related. Western-blot analyses of cultured oligodendrocytes and purified rat myelin showed only the 120,000 protein. Immunoprecipitation of iodinated membrane proteins of cultured oligodendrocytes also indicated the presence of only the 120,000 Mr protein. Deglycosylation of the 120,000 protein by N-glycanase resulted in a 110,000 protein. The immunoblot pattern suggested some similarities between oligodendrocyte adhesion molecules and the neural cell adhesion molecule (N-CAM). Therefore, the 120,000, 140,000, and 180,000 Mr proteins were compared to N-CAM by Western-blot analysis, immunofluorescence staining, and by immunoprecipitation. The results suggest that oligodendrocytes contain a 120,000 membrane glycoprotein that is related to N-CAM.

Animals↗

PubMed1999

Cdc42, Rac1, and their effector IQGAP1 as molecular switches for cadherin-mediated cell-cell adhesion.

Cell-cell adhesion is a dynamic process in various cellular and developmental situations. Cadherins, well-known Ca(2+)-dependent adhesion molecules, are thought to play a major role in the regulation of cell-cell adhesion. However, the molecular mechanism underlying the rearrangement of cadherin-mediated cell-cell adhesion is largely unknown. Cdc42 and Rac1, belonging to the Rho small GTPase family, have recently been shown to be involved in the regulation of cell-cell adhesion. In addition, IQGAP1, an effector for Cdc42 and Rac1, has been shown to regulate the cadherin function through interaction with beta-catenin, a molecule associated with cadherin. In this review, we will summarize the mode of action of Cdc42 and Rac1 as well as IQGAP1 as molecular switches for the cadherin function, and then discuss physiological processes in which the Cdc42/Rac1/IQGAP1 system may be involved.

Animals↗

PubMed1996

Immunohistochemical localization of cell adhesion molecules and cell-cell contact proteins during regeneration of the rat optic nerve induced by sciatic nerve autotransplantation.

BACKGROUND: The central nervous system neurons of adult mammals are known to regenerate into peripheral nerve autograft. The localization of cell adhesion molecules and cell-cell contact proteins were studied during axonal regeneration induced by sciatic nerve autotransplantation. METHODS: A sciatic nerve autograft was anastomosed to the proximal stump of the transected rat optic nerve. Immunofluorescence microscopy, thin sectioning, and immunoelectron microscopy with the preembedding method and ultrathin cryosections were used to localize cell adhesion molecules (L1; neural cell adhesion molecule, NCAM; myelin-associated glycoprotein, MAG) and cell-cell contact proteins (connexins 32, 43, ZO-1) at 3 days to 4 weeks postoperation. RESULTS: Most regenerating axons contacted astrocytes in the optic nerve and Schwann cells in the graft. Immunoreactivity of NCAM was widely distributed along the surface of axons, astrocytes, Schwann cells, and perineurial cells. The L1 immunoreactivity was confined to the interface of axon-astrocyte and of axon-Schwann cell. MAG immunoreactivity was seen at the interface of axon and myelin within the graft. Connexins 32, 43, and ZO-1 immunoreactivities were observed at contact sites between axons and Schwann cells within the graft. CONCLUSIONS: Cell adhesion molecules (L1, NCAM, MAG) are localized at the cell surface of regenerating axons, astrocytes, and Schwann cells during optic nerve regeneration elicited by peripheral nerve graft. Cell-cell contact proteins (connexins 32, 43, ZO-1) are present at the interface between axons and Schwann cells in the graft. Our results suggest that these molecules are involved in cell adhesion events during optic nerve regeneration.

Animals↗

PubMed1986

Dynamic expression of the cell adhesion molecule cell-CAM 105 in fetal and regenerating rat liver.

Cell-CAM 105 is an integral cell surface glycoprotein that is involved in cell-cell adhesion of adult rat hepatocytes in vitro. In the present report we used a radio-immunoassay, a quantitative immunoblotting technique and immunofluorescence microscopy to investigate the expression of cell-CAM 105 in fetal and regenerating rat liver. In the fetal liver cell-CAM 105 did not appear until day 16 of the gestation, when it increased rapidly to reach the level found in adult liver, 3 weeks after birth. In liver regenerating after partial hepatectomy a transient decrease in the amount of cell-CAM 105 was observed in the plasma membranes of the hepatocytes. A significant decrease was observed as early as 12 h after partial hepatectomy, reaching a minimum by 3 days after the operation, corresponding to approx. 35% of the amount of cell-CAM 105 in normal liver. The amount then increased slowly and was back to the normal level by about 15 days after partial hepatectomy. The results indicate that cell-CAM 105 exerts its major function in terminally differentiated cells. An excellent correlation was seen between the kinetics of the expression of cell-CAM 105 and of reported changes of both enzymatic and organizational patterns of hepatocytes in regenerating and fetal liver. This suggests that cell-CAM 105 could be important for the development and maintenance of the cell-cell binding and organizational pattern characteristic of terminally differentiated hepatocytes.

Adenosine Triphosphatases↗

PubMed2000

Quantitative evaluation of cell attachment to glass, polystyrene, and fibronectin- or collagen-coated polystyrene by measurement of cell adhesive shear force and cell detachment energy.

Quantitative evaluation of a material's affinity for cells is essential to understanding cell-material interaction inside a body and it is also necessary for the development of new biomaterials with superior biocompatibility. In the present study, the shear force and the total energy necessary to detach a single murine fibroblast L929 adhering to glass, polystyrene, and fibronectin- or collagen-coated polystyrene were measured directly by applying a lateral force, using a cantilever, to the cell. The projected area of the cell was also measured, and then cell adhesive shear strength and cell detachment surface energy were determined by dividing the shear force and the total energy by the area. Among these four materials, the cells on collagen-coated polystyrene have the highest cell adhesive shear strength and cell detachment surface energy (1500 Pa and 29 pJ on average, respectively), followed by the cells on fibronectin-coated polystyrene (1000 Pa and 16 pJ, respectively). The cells on glass and polystyrene had almost the same cell adhesive shear strength and cell detachment surface energy (420-670 Pa and 7-11 pJ, respectively). These observations suggest that cell adhesive shear strength and cell detachment surface energy depend on the number of the bindings between the cell and a material's surface rather than on the strength of each binding.

Animals↗