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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radioiodinated rat CNS axolemmal fragments adhered to cultured rat Schwann cells by a time-, temperature-, and concentration-dependent process independent of extracellular ionized calcium. Adhesion showed target and signal specificity; axolemmal fragments adhered to endoneurial or dermal fibroblasts to a much lesser extent than to Schwann cells, and plasma membrane fragments from skeletal muscle, erythrocytes, or PNS myelin adhered to Schwann cells to a lesser extent than did axolemmal fragments. Brief trypsinization removed 94 to 97% of bound radioactivity from Schwann cells previously incubated with 125I-axolemmal fragments for up to 24 hr, indicating that adhesion was largely a surface phenomenon rather than the result of rapid internalization of axolemmal fragments by the Schwann cells. When adhesion was compared to the axolemmal mitogenic response of Schwann cells, the concentration of axolemmal fragments yielding half-maximal adhesion was the same as the concentration producing half-maximal stimulation of Schwann cell mitosis. Trypsin digestion, homogenization, or heating of axolemmal fragments before application to cultured Schwann cells diminished adhesion and axolemmal fragment-induced stimulation of Schwann cell mitosis in a parallel fashion. Whereas adhesion of axolemmal fragments to the surfaces of the cultured Schwann cells reached completion within 4 hr in this assay system, induction of Schwann cell mitosis by the fragments required contact with Schwann cells for a minimum of 6 to 8 hr and reached a maximum when the axolemmal fragments had adhered to the Schwann cells for 24 hr or more.
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PMID:Adhesion of axolemmal fragments to Schwann cells: a signal- and target-specific process closely linked to axolemmal induction of Schwann cell mitosis. 397 72

Gametes of the unicellular green alga Chlamydomonas reinhardii recognize and adhere to cells of the opposite mating type by flagellar contact. Adhesion between these specialized organelles signals a rapid series of mating events which result in gamete fusion. The sequence of morphological changes (flagellar tip activation, cell wall loss, and mating structure elongation), which occur as a consequence of the sexual signalling, have been characterized. The signalling mechanisms have, however, not been defined. Calcium is known to be involved during fertilization of animal species. Increased intracellular free calcium, which can be achieved either by calcium influx or by mobilization of ions from intracellular stores, has been observed during activation of both eggs and sperm. A recent report by Bloodgood & Levin that gametes of C. reinhardii preloaded with 45Ca showed a transient increase in Ca efflux following mating, suggests that intracellular Ca redistribution may also accompany mating in this algal species. We have used X-ray microanalysis to analyze the subcellular distribution of bound calcium during mating in Chlamydomonas reinhardii. X-ray maps reveal that calcium is sequestered in discrete granules within the gamete cell body prior to mating and that during activation and cell fusion, calcium is diffuse throughout the cell. This suggests the possibility that calcium serves as a second messenger in this species.
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PMID:Intracellular calcium redistribution during mating in Chlamydomonas reinhardii. 404 49

Platelet vegetations or thrombi are common findings in subacute bacterial endocarditis. We investigated the hypothesis that human platelets selectively bind or adhere strains of Streptococcus sanguis and Streptococcus mutans and aggregate, as a result, into an in vitro thrombus. Earlier ultrastructural studies suggested that aggregation of platelets over time by Staphylococcus aureus was preceded in order by adhesion and platelet activation. We uncoupled the adhesion step from activation and aggregation in our studies by incubating streptococci with platelet ghosts in a simple, quantitative assay. Adhesion was shown to be mediated by protease-sensitive components on the streptococci and platelet ghosts rather than cell surface carbohydrates or dextrans, plasma components, or divalent cations. The same streptococci were also studied by standard aggregometry techniques. Platelet-rich plasma was activated and aggregated by certain isolates of S. sanguis. Platelet ghosts bound the same strains selectively under Ca2+- and plasma-depleted conditions. Fresh platelets could activate after washing, but Ca2+ had to be restored. Aggregation required fresh platelets in Ca2+-restored plasma and was inducible by washed streptococcal cell walls. These reactions in the binding and aggregometry assays were confirmed by transmission electron microscopy. Surface microfibrils on intact S. sanguis were identified. These appendages appeared to bind S. sanguis to platelets. The selectivity of adhesion of the various S. sanguis strains to platelet ghosts or Ca2+- and plasma-depleted fresh washed platelets was similar for all donors. Thus, the platelet binding site was expressed widely in the population and was unlikely to be an artifact of membrane aging or preparation. Since selective adhesion of S. sanguis to platelets was apparently required for aggregation, it is suggested that functionally defined receptors for ligands on certain strains of S. sanguis may be present on human platelets. Some differences in the selectivity and rate of the aggregation response were noted among platelet donors, although the meaning of the variability requires further study. Nonetheless, these interactions may contribute to platelet accretion in the initiation and development of vegetative lesions in the subacute bacterial endocarditis.
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PMID:Aggregation of human platelets and adhesion of Streptococcus sanguis. 618 97

Treatment of epithelial African green monkey kidney (BSC-1) cells with the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a rapid and reversible redistribution of actin and vinculin that is detectable after only 2 min of treatment. Within 20-40 min, stress fibers disappear, while at the same time large actin-containing ribbons resembling ruffles develop both at the cell periphery and in more central regions. Vinculin is associated with these actin ribbons or bands in a punctate or patchy staining pattern. Adhesion to the substratum is changed from predominantly focal contacts associated with stress fiber ends in untreated cells to broad zones of close contact after TPA treatment. High voltage electron microscopic observations disclose the ribbons to consist of highly cross-linked actin filament networks. Thus, association of vinculin with filament networks, rather than (the ends of) filament bundles, is demonstrated. The integrity of microtubules and vimentin filaments is not affected by TPA treatment, but their distribution is altered to conform with the highly distorted cell shape. The response to TPA is neither prevented nor modified by nocodazole-induced depolymerization or taxol-induced stabilization of microtubules. An intact intermediate filament network seems not required either since colcemid-induced collapse of vimentin filaments towards the nucleus does not affect the cell's response to TPA. Rapid redistribution of actin and vinculin also takes place in enucleated cells and in the presence of cycloheximide, but is prevented by dinitrophenol or oligomycin. TPA-induced cytoskeletal alterations are independent of fibronectin expression and not mimicked, modified, or prevented by calmodulin inhibitors or experimentally elevated levels of calcium and cyclic AMP. Thus the morphological response to TPA involves rapid redistribution of actin and vinculin independent of transcription and translation, fluctuations in the levels of calcium or cyclic AMP, or changes in the organization of microtubules, intermediate filaments, and fibronectin.
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PMID:A tumor promoter induces rapid and coordinated reorganization of actin and vinculin in cultured cells. 620 76

To understand the mechanism of Entamoeba histolytica adhesion, we characterized the binding of trophozoites to human erythrocytes (RBC) in suspension by measuring the kinetics of amoeba-RBC complex formation. Adhesion was very efficient, since most of the amoebae were complexed with RBC after only 5 min at 37 degrees C in mixtures containing 10(4) amoebae and 10(6) RBC per ml; the adhesion rate depended on amoeba and RBC concentrations, but not on the A, B, and O human blood groups, and was maximal at 37 degrees C and pH 7.3 in the presence of 4 mM Ca2+ and 1 mM Mg2+. Adhesion was prevented if trophozoites were fixed with glutaraldehyde, but only decreased slightly if RBC were previously fixed; it decreased in the absence of glucose and was inhibited as a function of the concentration of cytochalasin B and of the metabolic inhibitors bathophenanthroline and 8-hydroxyquinoline. From these results we conclude that E. histolytica adhesion is an active process that depends on the amoebal cytoskeleton and metabolic energy and on the mobility of both amoebal and RBC surface ligands.
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PMID:Adhesion of Entamoeba histolytica trophozoites to human erythrocytes. 628 91

The calcium-independent mechanism of cell adhesion was studied in normal and polyoma virus-transformed BHK cells. The degree of Ca2+-independent adhesion was greatly reduced in pyBHK cells, whereas CA2+-dependent adhesion occurred to the same degree as in BHK cells. This decrease was shown not to be caused by simple masking of the adhesion sites or by their altered sensitivity to trypsin. Adhesion-blocking antibodies were used to identify molecules responsible for Ca2+-independent adhesion. The antibodies precipitated surface molecules specific for adhesion-competent cells. These have tentatively been named CIDSBHK and CIDSpyBHK. Both were glycoproteins with respective apparent molecular weights of 120K and 125K. CIDSpyBHK incorporated 3H-glucosamine more than CIDSBHK did. Possible modification of the Ca2+-independent adhesion mechanism in pyBHK cells is discussed.
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PMID:Modification of the calcium-independent mechanism of cell adhesion in transformed BHK cells. 632 Oct 41

This review of retinal pigment epithelial (RPE) physiology pays tribute to Anthony L. F. Gorman, who introduced the author to the giant neuron of Anisodoris nobilis (the sea lemon) and cellular neurobiology. The RPE is an epithelial monolayer with tight junctions, which controls the environment of the photoreceptor outer segments. The apical and basal membranes have different electrical properties and generate a standing potential across the eye. The RPE helps maintain adhesion between the retina and the wall of the eye. Adhesion is weakened by cyanide, low pH or low calcium, but enhanced by ouabain or acetazolamide. The RPE transports water from the subretinal space toward the choroid. This water movement is inhibited by hypoxia or cyanide but enhanced by ouabain or acetazolamide. The c-wave of the electroretinogram is a composite of a cornea-positive wave produced by hyperpolarization of the apical RPE membrane and a cornea-negative wave produced by the Muller cells, both in response to the fall in extracellular potassium that follows illumination of the photoreceptors. The "light response" of the standing potential is produced by depolarization of the basal membrane of the RPE. These examples illustrate how principles of cellular neurophysiology can be applied to questions of clinical relevance.
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PMID:From sea lemons to c-waves. 632 7

Extra-embryonic endoderm cells from gastrulating chick embryos possess Ca2+-dependent and Ca2+-independent adhesive mechanisms. These cells also contain an endogenous beta-D-galactoside-binding lectin and cell surface receptors bearing galactose groups. The endogenous lectin inhibits cellular adhesion. To test whether the adhesive interactions involving lectin and galactose molecules are part of the Ca2+-independent or Ca2+-dependent adhesive mechanism, dissociated cells which were preincubated in beta-galactosidase were allowed to aggregate in the presence and absence of Ca2+ ions. Significant decreases in adhesion were observed in both cases. Cells were also allowed to aggregate in the presence and absence of Ca2+ ions when blastoderm lectin was present in the medium. Adhesion was decreased in both cases. The results suggest that cell surface galactose groups and the beta-D-galactoside-binding lectin are involved in Ca2+-independent adhesion.
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PMID:Calcium-independent adhesion of extra-embryonic endoderm cells from the early chick blastoderm is inhibited by the blastoderm beta-D-galactoside-binding lectin and by beta-galactosidase. 640 23

Adhesion of the obligate intracellular bacterium Chlamydia trachomatis to host cells is associated with a flux of Ca2+ across the cell membrane, and infection is enhanced by treatment of host cells with Ca2+ ionophore. The possibility that Ca2+ might interact with host cell Ca2+ regulatory proteins to promote chlamydial infection was investigated. Treatment of HeLa 229 cells with the calmodulin inhibitors pimozide, trifluoperazine, chlorpromazine, promethazine or haloperidol reduced chlamydial infectivity as measured by inclusion counting or the specific incorporation of [3H]threonine. The inhibitory effect was reversible, dose-related and shown to be associated with impairment of chlamydial adhesion and uptake by the host cells. This effect was clearly distinguished from the delayed maturation of chlamydiae due to continuous exposure to calmodulin inhibitors which may result from a decrease in the availability of high energy compounds from the host cells necessary for chlamydial growth. The possible mechanisms for calmodulin-mediated chlamydial endocytosis are discussed.
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PMID:Control mechanisms governing the infectivity of Chlamydia trachomatis for HeLa cells: the role of calmodulin. 642 68

Mechanisms of adhesion between tumor cells and hepatocytes, which are likely to play a role in liver metastasis formation, were studied in vitro. TA3 mammary carcinoma and MB6A lymphosarcoma cells were added to rat hepatocytes that had been cultured for 24 hours. Adhesion was quantified by counting adherent cells seen in sections of pelleted, Epon-embedded culture fragments. Adhesion of TA3, but not of MB6A cells, was inhibited by antibodies prepared from an antiserum raised against sinusoidal face-enriched liver plasma membranes. Detergent-solubilized liver components, affinity purified on immobilized inhibitory antibodies, neutralized inhibition, whereas a subfraction separated from this material with the use of immobilized noninhibitory antiliver antibodies had no neutralizing activity. Adhesion of MB6A but not of TA3 cells was inhibited by the calcium ionophore A23187 and the local anesthetic procaine. The calmodulin inhibitor trifluoperazine inhibited adhesion of MB6A cells more strongly than that of TA3 cells. Finally, adhesion of TA3 cells was dependent on external calcium, whereas in the case of MB6A cells calcium could be replaced by magnesium. These observations suggested that adhesion of the two tumor cell types to hepatocytes involved distinct hepatocyte surface molecules and required distinct biochemical machinery.
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PMID:Adhesion of tumor cells to hepatocytes: different mechanisms for mammary carcinoma compared with lymphosarcoma cells. 643 81


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