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)

Thrombospondin is a 420-kD platelet alpha-granule glycoprotein that binds specifically to heparin. We examined adhesion to thrombospondin of CHO K1 cells and three mutant CHO lines with varying deficiencies in glycosaminoglycan (GAG) synthesis. In an experiment in which the parent line (K1) had 78% adherence to thrombospondin adsorbed to tissue culture plastic, CHO S745 cells, with less than 6% normal GAG synthesis had 11% adherence. CHO S677 cells, with decreased heparan sulfate proteoglycan but increased chondroitin sulfate proteoglycan, had 42% adherence. CHO S803 cells, with decreased heparan sulfate proteoglycan and normal chondroitin sulfate proteoglycan, had 31% adherence. Heparin inhibited K1 cell adhesion to thrombospondin, but not fibronectin, in a concentration-dependent manner. Dermatan sulfate but not chondroitin sulfate was also inhibitory. There was markedly decreased K1 cell adhesion to a thrombospondin core fragment that lacked the heparin binding NH2-terminal domain. Purified heparin binding domain, although poorly adhesive when adsorbed to substratum, inhibited cell adhesion to intact thrombospondin. Adhesion was better for all cell lines tested, including three human tumor cell lines, when thrombospondin was adsorbed at pH 4.0 compared with pH 7.4. When adsorption of thrombospondin was done at pH 7.4, cell adhesion was better when thrombospondin was adsorbed in the presence of greater than or equal to 0.6 mM calcium, compared to 0.1 mM calcium or EDTA. These findings suggest that thrombospondin can adsorb to plastic with varying degrees of exposure of a cell adhesion domain. We conclude that the thrombospondin cell adhesion receptor on CHO cells is a heparan sulfate proteoglycan, and that cell adhesion to thrombospondin depends on conformation of adsorbed thrombospondin.
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PMID:Chinese hamster ovary cell adhesion to human platelet thrombospondin is dependent on cell surface heparan sulfate proteoglycan. 252 6

An ischemic bowel model was used to stimulate adhesion formation in eight ponies. Heparin (40 USP u/kg) or saline was administered intravenously at surgery and was continued subcutaneously every 12 hours for 48 hours to evaluate the efficacy of heparin in preventing intraabdominal adhesions. Ponies were euthanatized after 6 weeks, and postmortem examinations were performed. A statistically significant difference was found between the heparin-treated and the control groups. Adhesions developed in three of four control ponies, and adhesions did not develop in three of four heparin-treated ponies. None of the adhesions resulted in clinical disease. In this study, heparin decreased the formation of adhesions in ponies after experimentally induced intestinal ischemia.
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PMID:Prevention of intraabdominal adhesions in ponies by low-dose heparin therapy. 350 82

Heparin inhibited monolayer adhesion of washed human and rabbit platelets to collagen-coated glass at 2.5 and 20 units/ml concentration, in the absence of red cells. Adhesion of rabbit platelets to de-endothelialized rabbit aorta, under similar conditions, was less strongly inhibited but no inhibition was seen at 40% haematocrit. Addition of plasma reduced, rather than enhanced heparin activity and hirudin 0.5 units/ml had no significant effect. Heparin also inhibited platelet aggregation, release of (14C) 5-HT and production of malondialdehyde in response to collagen and thrombin. Inhibition of thrombin-induced activity was greater in the presence of plasma. However, heparin enhanced aggregation and release evoked by ADP and did not consistently inhibit MDA synthesis produced by arachidonate. The results indicate that in addition to the effects of heparin on platelet function mediated by anti-thrombin activity and the previously described augmentation of responses to ADP, heparin has weak inhibitory activity against platelet-collagen interactions. Binding of heparin to the platelet membrane (and to surfaces to which platelets adhere) could account for these findings by causing non-specific interference with agonist-receptor interactions.
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PMID:Effect of heparin on platelet monolayer adhesion, aggregation and production of malondialdehyde. 710 Dec 45

Cell adhesion to amino acids 2179-2198 (SN-peptide) of the laminin-1 alpha1-chain is required for lung alveolar formation in vitro (M. L. Matter and G. W. Laurie. J. Cell Biol. 124: 1083-1090, 1994). The nature of the SN-peptide receptor(s) was probed with neutralizing anti-integrin monoclonal antibodies (MAb), cells lacking integrin subunits, soluble heparin, and SN-peptide columns. Cell adhesion and spreading studies confirmed the specificity of SN-peptide and revealed adhesion to be unaffected by inclusion of anti-beta1-, anti-alpha(2-6)- or anti-alpha(V)beta5-integrin MAb. Cells lacking beta1- or alpha6-integrin subunits were fully adherent. Adhesion was heparin, but not chondroitin sulfate or heparinase, sensitive, much as is alpha-dystroglycan-laminin-1 binding. Heparin eluted approximately 155- and 180-kDa cell-surface proteins from SN-peptide columns. An additional approximately 91-kDa protein was eluted by EDTA. All were unrecognized by anti-beta1-integrin MAb. SN-peptide therefore interacts with three cell-surface proteins for which the identity remains to be determined.
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PMID:Laminin E8 alveolarization site: heparin sensitivity, cell surface receptors, and role in cell spreading. 912 7

Heparin-binding forms of vitronectin, a multifunctional adhesive glycoprotein, are associated with the extracellular matrix (ECM) at different locations in the body and serve to promote cell adhesion and the regulation of pericellular proteolysis at sites of angiogenesis. In the present study we characterized the interactions of vitronectin with the counter-adhesive protein osteonectin (also termed SPARC or BM40). Osteonectin and vitronectin were both found associated with the ECM of cultured endothelial cells and were localized in vessel wall sections of kidney tissue. In vitro, the heparin-binding multimeric isoform of vitronectin bound to immobilized osteonectin in a saturable manner with half-maximal binding at 30-40 nM. Preincubation of plasma vitronectin with plasminogen activator inhibitor 1 (PAI-1), which provoked multimer formation, induced the binding of vitronectin to osteonectin. Binding was optimal at physiological ionic strength, and binary complexes were stabilized by tissue transglutaminase-mediated cross-linking. In a concentration-dependent fashion, PAI-1, CaCl2, heparin and heparan sulphate, but not other glycosaminoglycans, interfered with the binding of vitronectin to osteonectin. Using vitronectin-derived synthetic peptides as well as mutant forms of recombinant osteonectin, we found that the heparin-binding region of vitronectin interacted with the C-terminal region of osteonectin that contains a high-affinity Ca2+-binding site with counter-adhesive properties. Adhesion of cultured endothelial cells was partly abrogated by osteonectin and was correspondingly reversed by vitronectin in a concentration-dependent manner. These results indicate that specific interactions between vitronectin and osteonectin modulate cell adhesion and might thereby regulate endothelial cell function during angiogenesis.
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PMID:Differential modulation of cell adhesion by interaction between adhesive and counter-adhesive proteins: characterization of the binding of vitronectin to osteonectin (BM40, SPARC). 916 72

Adhesion of staphylococcal cells to intraocular lenses coated with heparin was studied under in vitro flow conditions (280 microl min(-1)) at 37 degrees C. The intraocular lenses were incubated with human cerebrospinal fluid for 1 h or with cerebrospinal fluid including 0.50% plasma for 12 h, prior to bacterial challenge. Two strains of Staphylococcus epidermidis selected for this study, were isolated from biomaterial-associated infections. Bacterial adhesion was quantitated by bioluminescence and visualized by fluorescence microscopy of acridine orange stained bacteria. Surface coating with heparin significantly decreased bacterial adhesion of both strains after incubation with cerebrospinal fluid including 0.50% plasma for 12 h (p = 0.0209). However, no difference in bacterial adhesion was obtained between intraocular lenses with and without heparin, after incubation with cerebrospinal fluid for 1 h (p = 0.327). Microscopy showed that more bacteria were present on intraocular lenses without heparin than on intraocular lenses with heparin. The results show that preincubation with a proteinaceous fluid influences subsequent bacterial adhesion to the polymer surface. The results suggest that IOLs with heparin coating may be less prone to bacterial adhesion under perfusion conditions after surface conditioning in human CSF with 0.50% plasma and a preincubation period of 12 h. Heparin coating might be a valuable tool to decrease implant-associated bacterial endophthalmitis.
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PMID:A new model to assess staphylococcal adhesion to intraocular lenses under in vitro flow conditions. 985 83

Enoxaparin is a low molecular weight heparin, widely accepted as anticoagulant or antithrombotic drug, and is likely to have a role in acute inflammation. To evaluate the anti-inflammatory potential of enoxaparin, we investigated the direct effect of the drug on the activation of endothelial cells. For this purpose we set up an in vitro system in which cultured valvular endothelial cells (VEC) activated by tumor necrosis factor alpha or lipopolysaccharide were exposed to a monocytic cell line; these conditions induced a significant adhesion of monocytes to VEC. Adhesion assays, ELISA, and flow cytometric analysis revealed that pretreatment with enoxaparin, at a relevant plasma concentration (16 microg/ml), acts upon activation of VEC by inhibition of lipopolysaccharide-induced E-selectin expression and tumor necrosis factor stimulated ICAM-1 expression, thus reducing monocyte adhesion to VEC. These results suggest a novel function of enoxaparin, namely to protect VEC from activation and inhibiting the expression of cell adhesion molecules.
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PMID:A novel attribute of enoxaparin: inhibition of monocyte adhesion to endothelial cells by a mechanism involving cell adhesion molecules. 1190 Dec 99

Endothelial lipase (EL), a new member of the lipoprotein lipase gene family, plays a central role in high density lipoprotein metabolism. Previous studies indicated that EL is expressed in endothelial cells, macrophages, and smooth muscle cells in atherosclerotic lesions in human coronary arteries. However, the functional role of EL in the local vessel wall remains obscure. In this study, we evaluated the ability of EL to modulate monocyte adhesion to the endothelial cell surface. EL mRNA and protein levels were markedly increased in tissues of the mouse model of inflammation induced by lipopolysaccharide injection. Adhesion assays in vitro revealed that overexpression of EL in COS7 or Pro5 cells enhanced monocyte bindings to the EL-expression cells. Heparin or heparinase treatment inhibited EL-mediated increases of monocyte adhesion in a dose-dependent manner. Moreover, ex vivo adhesion assays revealed that the number of adherent monocytes on aortic strips was significantly increased in EL transgenic mice and decreased in EL knock-out mice as compared with wild-type mice. These results suggest that EL on the endothelial cell surface can promote monocyte adhesion to the vascular endothelium through the interaction with heparan sulfate proteoglycans. Thus, the up-regulation of EL by inflammatory stimuli may be involved in the progression of inflammation.
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PMID:Endothelial lipase modulates monocyte adhesion to the vessel wall. A potential role in inflammation. 1548 5

The study was carried out on 40 apparently clinical healthy dogs classified into 5 groups of 8 dogs each. Adhesion was experimentally induced by transsection and reanastomosis of jejunum. In the control group the site of anastomosis and abdominal cavity was lavaged with 250 ml saline solution. In group two lavage was done with 250 ml of a liquid barrier composed of a combination of high molecular weight solution (1% sodium carboxymethylcellulose) as a carrier, non-steroidal anti-inflammatory drug (Piroxecam), broad spectrum antibiotic (Cephalosporin), anticoagulant (Heparin) and antioxidant (0.5% methylene blue). In group three the anastomosis site was covered with a sodium hyalouronate/carboxymethylcellulose bioresorbable membrane (Seprafilm). In group four a natural biocompatible collagen sheet (VET BIO SIS T) was applied on the anastomosis site. In group five the abdominal cavity was lavaged with 250 ml liquid barrier and the anastomosis site was covered by either Seprafilm membrane or VET BIO SIS T sheet. At the fourteen day after operation, adhesion was assessed by ultrasonography after instillation of 1000 ml of physiological saline solution into the abdominal cavity. The dogs were sacrificed and an autopsy examination was carried out with the attention to the number, density and site of the adhesion formation. The results revealed that all the control dogs and some dogs in the treatment groups had positive ultrasonographic findings. Transabdominal sonogram clearly showed echogenic bands floating in the abdominal cavity and echogenic masses in more serious subjects. Necropsy examination showed that all the control dogs had intra-abdominal adhesions (8 of 8 dogs) and treatment with liquid barrier (4 of 8 dogs), seprafilm membrane barrier (3 of 8 dogs), VET BIO SIS T sheet barrier (4 of 8 dogs) and combination of fluid and membrane barrier groups (4 of 8 dogs) significantly (p < 0.05) reduced the incidence of adhesion formation. The adhesion severity in the four treated groups was significantly (p < 0.05) decreased compared with the control group as shown by both ultrasonography and necropsy examination scores. In conclusion the suggested hypothesis is more or less positive and the combined liquid and membrane barriers might be an effective way to decrease intra-abdominal adhesion formation, and the ultrasonography is a useful tool to diagnose intra-abdominal adhesion, and their applications might be valuable to the clinical settings.
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PMID:The effects of combined liquid and membrane barriers in prevention of post-operative intra-abdominal adhesions after experimental jejunal anastomosis in dogs. 1571 69

This study was conducted to determine the probability of adhesion formation with certain materials after abdominopelvic surgery, and to assess the effectiveness of adhesion-preventing agents. The study included 2 phases. In the first phase of the study, 50 rats that had been divided into 5 groups were examined. Group 1 served as the control group. In group 2, 2 mL blood was taken from the femoral vein of the rat; in group 3, 0.0625 g talcum powder was mixed with 2 mL saline; in group 4, 2 mL ileal content was identified; and in group 5, 2 mL cecal content had spilled into the peritoneum. In the second phase of the study, 50 rats that had been divided into 5 groups were examined. Ileal content was the leading cause of intraperitoneal adhesions in the first phase; in the second phase, in group 1, 2 mL ileal content and 5 mL povidone-iodine (10%) were used; in group 2, 2 mL ileal content and 5000 units aprotinin were mixed with 5 mL saline; in group 3, 2 mL ileal content and 25 IU heparin (5000 IU/L) were mixed with 5 mL saline; in group 4, 2 mL ileal content and 5 mL 32% dextran 70 were combined; and in group 5, 2 mL ileal content was used together with 5 mL Ringer's lactate. On postoperative day 14, the rats were killed with the use of high-dose intramuscular ketamine, and necropsies were performed on all rats. Adhesions were most often established because of ileal and cecal contents. Blood and talcum powder produced less adhesion formation. Heparin and 32% dextran 70 were significantly more effective at preventing adhesion formation due to ileal contents. Intraperitoneal heparin and 32% dextran 70 may be particularly valuable for the prevention of adhesions due to intestinal content in cases with no contraindications.
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PMID:Effectiveness of treatment to prevent adhesions after abdominal surgery: an experimental evaluation in rats. 1790 Oct 28


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