Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five strains of lactobacilli were tested for their ability to adhere to human enterocyte-like Caco-2 cells in culture. Seven Lactobacillus strains adhered well to the Caco-2 cells, of which three possessed calcium-independent adhesion properties. A high level of calcium-independent adhesion was observed with the human stool isolate Lactobacillus acidophilus strain LB. Scanning electron microscopy revealed that this strain adhered to the apical brush border of the cells. Adhesion increased in parallel with the morphological and functional differentiation of the Caco-2 cells. Two Lactobacillus components were involved in this adhesion. One was protease-resistant and bacterial-surface-associated; the other was heat-stable, extracellular and protease-sensitive.
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PMID:Adhesion of human Lactobacillus acidophilus strain LB to human enterocyte-like Caco-2 cells. 152 9

When coated on bacteriological plastic at doses greater than or equal to 0.1 microgram/cm2, human and bovine angiogenin support calf pulmonary artery endothelial and Chinese hamster fibroblast cell adhesion and spreading, but do not affect cell adhesion when in solution. The kinetics of endothelial cell attachment to angiogenin are indistinguishable from those in the presence of gelatin. Calcium and/or magnesium ions are critical for cell adhesion or spreading onto angiogenin but protein synthesis and glycoprotein secretion are not necessary. Adhesion to angiogenin is not altered by the addition to the incubation solution of fibronectin, fibrinogen, laminin, collagen I and IV, or vitronectin. The peptide Arg-Gly-Asp-Ser inhibits endothelial cell response to angiogenin whereas the reverse peptide Ser-Asp-Gly-Arg-Gly has no effect. These findings show that angiogenin can serve as an effective substratum for cell adhesion by inducing an interaction similar to but independent from that of other extracellular matrix molecules. Induction of cell adhesion and subsequent migration may be critical steps in the process of angiogenesis.
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PMID:Angiogenin supports endothelial and fibroblast cell adhesion. 154 88

1. A mesodermal stem cell line C3H10T1/2 was induced to differentiate to muscle by adding 0.3 microM-5-aza-2'-deoxy-cytidine to the medium for 24 h. The changes in membrane currents during differentiation were studied by whole-cell recording and changes in the expression of fibronectin, Neural Cell Adhesion Molecule (NCAM), myosin and desmin were studied immunohistochemically. 2. The stem cells showed the morphology of fibroblastic cells. Most of the stem cells showed ATP-induced slow K+ current. T-type Ca2+ current and inward rectifier K+ current were observed in 19% of the stem cells. The stem cells expressed fibronectin, but not NCAM, myosin or desmin. 3. About 2 weeks after the addition of 5-aza-2'-deoxy-cytidine, large multinucleated skeletal muscle-like cells appeared. Most of the induced muscles showed L-type Ca2+ current, responses to acetylcholine, outward K+ current, inward rectifier K+ current and contraction upon depolarizing stimulation. They expressed NCAM, myosin and desmin, but not fibronectin, and showed no ATP response. 4. In some batches (2/14), the induced muscles showed spontaneous twitches, and possessed tetrodotoxin (TTX)-sensitive Na+ current in addition to the currents described above. Furthermore clear striation was observed in some of the twitching muscles under Nomarski optics. 5. To ascertain the properties of cells at the initial step of muscle differentiation, whose differentiation is determined but not yet evident morphologically or electrophysiologically, subcloning was performed from the heterogeneous cells 10 days after induction. Three myogenic clones were obtained, which proliferated at low cell densities but differentiated to muscle with a high incidence at high cell densities, as well as ten non-myogenic clones. 6. Most myogenic clones still showed ATP-induced K+ current and fibronectin. In addition, most of them showed T-type Ca2+ current and inward rectifier K+ current. They had already expressed NCAM. No other properties observed in muscles had yet been expressed. Most cells of the non-myogenic clones showed ATP-induced K+ current and fibronectin. T-type Ca2+ current was also expressed, but not inward rectifier K+ current or NCAM. 7. The properties of the observed ionic currents were studied. The TTX-sensitive Na+ current could be completely blocked by 0.1 microM-TTX. It could be evoked by depolarizing steps to a level above -40 mV, while steady-state inactivation was detectable around -75 mV and reached half by -52 mV. T-type Ca2+ current could be evoked by a depolarizing pulse to a level above -45 mV, with a maximum amplitude around -15 mV.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Electrophysiological and immunohistochemical analysis of muscle differentiation in a mouse mesodermal stem cell line. 166 64

Adhesion of circulating leukocytes to the vascular endothelium during inflammation is mediated in part by their interaction with the endothelial-leukocyte adhesion molecule ELAM-1. ELAM-1, a member of the LEC-CAM family of cell adhesion molecules, expresses an N-terminal carbohydrate recognition domain (CRD) homologous to various calcium-dependent mammalian lectins. However, the contribution of the CRD to cell adhesion and its carbohydrate binding specificity have not been elucidated. This study demonstrates that transfection of a human fucosyltransferase cDNA into nonmyeloid cell lines confers ELAM-1--dependent endothelial adhesion. Binding activity correlates with de novo cell surface expression of the sialylated Lewis x tetrasaccharide, whose biosynthesis is determined by the transfected fucosyltransferase cDNA. We propose that specific alpha(1,3)fucosyltransferases regulate cell adhesion to ELAM-1 by modulating cell surface expression of one or more alpha(2,3)sialylated, alpha(1,3)fucosylated lactosaminoglycans represented by the sialyl Lewis x carbohydrate determinant.
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PMID:ELAM-1--dependent cell adhesion to vascular endothelium determined by a transfected human fucosyltransferase cDNA. 169 67

The acute inflammatory response requires that circulating leukocytes bind to and penetrate the vascular wall to access the site of injury. Several receptors have been implicated in this interaction, including a family of putative carbohydrate-binding proteins. We report here the identification of an endogenous carbohydrate ligand for one of these receptors, endothelial-leukocyte adhesion molecule 1 (ELAM-1). Radiolabeled COS cells transfected with a plasmid containing the cDNA for ELAM-1 were used as probes to screen glycolipids extracted from human leukocytes. COS cells transfected with this plasmid adhered to a subset of sialylated glycolipids resolved on TLC plates or adsorbed on polyvinyl chloride microtiter wells. Adhesion to these glycolipids required calcium but was not inhibited by heparin, chondroitin sulfate, keratan sulfate, or yeast phosphomannan. Monosaccharide composition, linkage analysis, and fast atom bombardment mass spectrometry of the glycolipids indicate that the ligands for ELAM-1 are terminally sialylated lactosylceramides with a variable number of N-acetyllactosamine repeats and at least one fucosylated N-acetylglucosamine residue.
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PMID:Carbohydrate ligands for endothelial-leukocyte adhesion molecule 1. 170 26

Adhesion of human neutrophils to endothelial cells is a crucial step during migration to the extravascular sites of inflammation. A large number of molecules, including the CD44 and LAM-1 antigens, have been described to participate in this process. We have investigated the regulation by human recombinant tumor necrosis factor-alpha (TNF-alpha) of human neutrophil plasma membrane expression of both CD44 and LAM-1 adhesion molecules, as well as that of CD43 sialophorin, which has been involved in adhesion and activation of leukocytes. The expression of these three antigens was down-regulated in neutrophils upon TNF-alpha treatment, as determined by immunofluorescence and immunoprecipitation experiments. However, the expression of other cell surface molecules, such as CD45 or CD11b, was up-regulated. Similar regulatory effects were also observed upon neutrophil treatment with other activating agents such as the chemoattractant peptide formyl-Met-Leu-Phe, the calcium ionophore A23187, or the phorbol ester phorbol 12-myristate 13-acetate. Protease inhibitors virtually abrogated the TNF-alpha-induced down-regulation of CD43 and CD44 expression, but not that of LAM-1, suggesting the involvement of a protease activity in this process. These results underline the role of TNF-alpha on the differential regulation of cell surface expression of neutrophil adhesion molecules, thus implying modifications in the neutrophil adhesive properties.
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PMID:Down-regulation by tumor necrosis factor-alpha of neutrophil cell surface expression of the sialophorin CD43 and the hyaluronate receptor CD44 through a proteolytic mechanism. 172 Oct 26

The adhesion of platelets to purified laminin under flow conditions was investigated. Adhesion to laminin was strongly dependent on the presence of divalent cations. In the absence of cations platelet adhesion (8% coverage in 5 minutes) was maximal at a shear rate of 100/s and no adhesion could be detected at shear rates above 800/s. In the presence of 0.8 mmol/L Mg2+ and 2 mmol/L Ca2+ platelet adhesion reached its maximum (30% coverage) around 800/s. At 1,800/s platelets still adhered to purified laminin (coverage of 6%). Antibodies against the E8 domain of laminin and antibodies against the alpha 6 and beta 1 chains of platelet membrane glycoprotein very late activation antigen-6 (VLA-6), completely inhibited adhesion. No inhibition was found with antibodies against glycoprotein IIb:IIIa, against the alpha 2 chain of VLA-2, and against the alpha 5 chain of VLA-5. Fibronectin and von Willebrand factor were not involved in laminin-dependent adhesion. Anti-VLA-6 partly inhibited platelet adhesion to the extracellular matrix of endothelial cells at shear rates below 800/s. Preincubation of the matrices with antilaminin E8 antibodies did not influence the adhesion. These results show that purified laminin supports platelet adhesion and that the presence of VLA-6 is important for platelet adhesion under flow conditions. The protein in the matrix with which VLA-6 interacts is currently unknown.
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PMID:Platelet adhesion to laminin: role of Ca2+ and Mg2+ ions, shear rate, and platelet membrane glycoproteins. 173 1

1. Electrophysiological and immunohistochemical properties during the early stages of muscle differentiation were studied in two myoblastic cell lines, mouse C2C12 and rat L6, and compared to those in myogenic clonal cells derived from the mouse mesodermal stem cell line C3H10T1/2, studied in the preceding paper. 2. Mouse C2C12 cells were induced to differentiate to muscle by changing from 10% fetal calf serum to 2% horse serum in the medium. Most of the C2C12 cells before serum reduction showed ATP-induced slow K+ current. Twelve per cent showed inward rectifier K+ current. They expressed fibronectin and Neural Cell Adhesion Molecule (NCAM). Small spindle-shaped cells at an early stage of muscle differentiation began to appear 24 h after serum reduction. In contrast to cells before serum reduction, only 13% of these spindle-shaped cells showed an ATP response. Most showed tetrodotoxin (TTX)-resistant Na+ current and outward K+ current. Thirty-eight per cent had inward rectifier K+ current. They expressed NCAM but not fibronectin. The T-type Ca2+ current was not observed up to the latest stage of differentiation investigated. 3. Rat L6 cells in maintaining culture medium showed only infrequent ATP responses, but already showed TTX-resistant Na+ current. No clear T-type Ca2+, inward rectifier K+ or outward K+ currents were observed. About one-third of the cells did not express fibronectin. From these results, L6 cells appear to be at a stage near to but slightly earlier than that of C2C12 cells after serum reduction. 4. The properties of the early stages of muscle differentiation in C3H10T1/2 cells, such as the disappearance of ATP-induced K+ current and fibronectin, and the appearance of NCAM, were also seen in C2C12 and L6. However, T-type Ca2+ and inward K+ currents, which were found in the initial stages of C3H10T1/2 muscle differentiation, were not clearly observed in C2C12 and L6. Instead, C2C12 and L6 showed a TTX-resistant Na+ current which was never observed in C3H10T1/2 cells. 5. The properties of the TTX-resistant Na+ current were investigated. In L6 cells, it was reduced to 60% by 1 microM-TTX. It could be evoked by depolarizations to a level above -50 mV with a maximum amplitude at around -15 mV. Steady-state inactivation was detectable with pre-pulses to -100 mV for 100 ms and reached half at pre-pulses of -78 mV. These parameters of inactivation are clearly different from those of the TTX-sensitive Na+ current observed in C3H10T1/2-derived mature muscle cells in the preceding paper.
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PMID:Comparison of initial stages of muscle differentiation in rat and mouse myoblastic and mouse mesodermal stem cell lines. 179 50

The adhesion of osteoclasts to the bone matrix is mandatory for bone resorption. Contact of the osteoclast with bone surface induces, in fact, cell polarization and organization of the resorbing apparatus, the so-called "ruffled border." Cell-matrix interaction in osteoclasts is a complex phenomenon resulting from formation of the "clear zone," a cytoplasmic area presenting the adhering plasma membrane, or "sealing membrane." The sealing membrane surrounds the ruffled border and seals the resorbing compartment, namely the extracellular space in which bone resorption takes place. Adhesion at this level occurs via specialized discrete structures, the "podosomes." Podosomes present most of the protein commonly found in focal adhesions, but with a peculiar organization. They are dynamic elements suitable for regulation, according with the functional demand of the cell. Their assembly increases during bone resorption and is regulated by the cytosolic free calcium concentration and the activity of protein kinase C.
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PMID:Clear zone in osteoclast function: role of podosomes in regulation of bone-resorbing activity. 185 48

Cerebral involvement in Plasmodium falciparum malaria is associated with sequestration of infected red blood cells and occlusion of cerebral vessels. Adhesion of infected erythrocytes along the vascular endothelium as well as binding of uninfected erythrocytes to cells infected with late-stage asexual parasites (rosetting) may be important in erythrocyte sequestration. We report that the recently discovered rosetting phenomenon shares characteristics with other human cell-cell interactions (heparin sensitivity, temperature independence, Ca2+/Mg2+ and pH dependence). Mono- and polyclonal antibodies specific for PfHRP1, a histidine-rich protein present in the membrane of P. falciparum-infected erythrocytes, disrupt rosettes but do not affect attachment of infected erythrocytes to endothelial cells. The inhibitory anti-PfHRP1 antibodies reacted with rosetting parasites in indirect immunofluorescence and with P. falciparum polypeptides of Mr 28,000 and Mr 90,000 in immunoprecipitation and immunoblotting, respectively. No inhibitory effects on erythrocyte rosetting were obtained with antibodies to related histidine-rich or other antigens of P. lophurae or P. falciparum. Whether the epitope that mediates rosetting, and is recognized by the anti-PfHRP1 antibodies, is located on PfHRP1 or on a crossreactive antigen remains to be established. The results suggest that endothelial cytoadherence and erythrocyte rosetting involve different molecular mechanisms.
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PMID:Antibodies to a histidine-rich protein (PfHRP1) disrupt spontaneously formed Plasmodium falciparum erythrocyte rosettes. 210 39


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