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

We have previously reported that fibrinogen/fibrin can induce the migration of vascular smooth muscle cells in vitro. In this study, we examined the effect of substrate-bound fibrinogen/fibrin and other cell attachment-promoting proteins on the adhesion of vascular smooth muscle cells. The amount of fibrinogen/fibrin adsorbed to plastic wells and the adhesion of smooth muscle cells to the wells were found to depend on the concentration of fibrinogen used for coating the wells. The effect of fibrinogen/fibrin was comparable to that of so-called cell attachment-promoting proteins (fibronectin, vitronectin, and type I collagen). Adhesion of smooth muscle cells to fibrinogen/fibrin-coated wells was inhibited by the synthetic peptide GRGDS, but not by a control peptide, GRGES. Vitronectin, fibronectin, type I collagen, denatured type I collagen and commercial gelatin also induced smooth muscle cell adhesion. The adhesion induced by vitronectin, denatured type I collagen, and commercial gelatin was inhibited by GRGDS. However, the adhesion induced by type I collagen was not influenced and that induced by fibronectin was only slightly inhibited. These observations suggest that fibrinogen/fibrin deposited extracellularly in the arterial intima may act as a scaffold in the process of smooth muscle cell migration.
Atherosclerosis 1992 Oct
PMID:Substrate-bound fibrinogen, fibrin and other cell attachment-promoting proteins as a scaffold for cultured vascular smooth muscle cells. 128 31

Leukocyte adhesion and other injury parameters have been studied in the aortic endothelium of Sprague-Dawley rats in two situations: (1) spontaneous pathology in conventional rats with antibodies to Mycoplasma pulmonis and/or Kilham or Sendai viruses, and (2) intravascular coagulation by thrombin administration in SPF rats. Adhesion (esterase (+) leukocytes/mm2) in SPF rats was 8 +/- 5 (n = 12). Adhesion in 38% of the conventional rats was 54 +/- 27 (n = 8), half of them being non-analyzed and the rest having antibodies to M. pulmonis and/or Kilham rat virus. In 19 rats with antibodies to M. pulmonis and/or Kilham or Sendai viruses, AgNO3 and hematoxylin staining of the aortic endothelium showed an increase in leukocyte adhesion, and the presence of argyrophilic cells, stigmata and granularity--severe endothelial lesions being observed in some cases. Adhesion in rats after 0.25, 1, 3 and 6 h of thrombin administration (30 units/100 g) was not different from controls. Adhesion after 24 h was 108 +/- 53 (n = 10) and 60 +/- 59 (n = 10), and 22 +/- 20 (n = 10) in rats treated with thrombin plus heparin or hirudin, respectively. Thrombin produced endothelial lesions at all times studied, and these included membrane blebs, platelet and erythrocyte adhesion and alterations in the pattern of endothelial esterase activity.
Atherosclerosis 1992 Apr
PMID:Effect of spontaneous pathology and thrombin on leukocyte adhesion to rat aortic endothelium. 159 Aug 26

Adhesion of monocytes to the arterial endothelium is an important early event in atherosclerosis. Several lines of evidence have suggested that oxidation of low density lipoprotein (LDL) in the arterial wall may initiate the inflammatory-like process that generally is present in atherosclerotic lesions. In vitro, oxidation of LDL can be obtained both by exposure to divalent ions, such as Cu2+, or by incubation with different cell types, including monocytes and endothelial cells. The present study was designed to investigate the possible influence of oxidized LDL on the adhesive properties of endothelial cells. We report here that Cu(2+)-oxidized LDL is as effective as interleukin 1 beta in stimulating the ability of cultured human endothelial cells to bind U937 monocytic cells. The stimulation was inhibited by cycloheximide, indicating that de novo protein synthesis is required. Biologically modified LDL, obtained by incubation with human peripheral blood monocytes, also enhanced the adhesiveness of endothelial cells. This effect was not due to an increased secretion of interleukin 1 beta from the monocytes exposed to LDL. Treatment of endothelial cells for 24 h with native LDL was also found to increase the adhesion of U937 cells. Exposure of endothelial cells to LDL for 24 h resulted in an oxidative modification of LDL. Furthermore, the antioxidant butylated hydroxytoluene inhibited both the endothelial-dependent oxidation of LDL as well as the increased adhesion of U937 cells, suggesting a coupling between these two processes. The results indicate that LDL, modified by exposure to monocytes or endothelial cells in the arterial wall, may increase the adhesive properties of the endothelium.
Atherosclerosis 1991 Oct
PMID:Biologically modified LDL increases the adhesive properties of endothelial cells. 168 6

Monocyte adhesion to endothelium is believed to be an initiating event in atherosclerosis both in arteries and in saphenous vein coronary artery bypass grafts. We have developed a method to quantify adhesion of 51Cr-labelled human blood monocytes to saphenous vein. Adhesion to the intimal surface was measured to uniform 6 mm diameter discs, the adventitia of which was embedded in a layer of inert silicone grease. The identity, number and location of bound cells was further defined by scanning electron microscopy. The proportion of monocytes adhering to discs of freshly-isolated vein was 7.1 +/- 1.2% (SE, n = 8), which was equivalent to 500 +/- 80 monocytes/mm2. The percentage of monocytes adhering was independent of the number of monocytes added in the range 5-50 x 10(4). Scanning micrographs showed 80% endothelial coverage with monocytes adhering preferentially but not exclusively to subendothelium. Endothelial removal increased monocyte adhesion by 1.60 +/- 0.15-fold (n = 8, P less than 0.01). Vein surgically prepared for use in coronary bypass surgery, had a 50% reduction in endothelial coverage and a small but non significant (1.14 +/- 0.13-fold, n = 8) increase in monocyte adhesion. Treatment of freshly-isolated vein for 4 h at 37 degrees C with 1 micrograms/ml of E. Coli endotoxin followed by extensive washing did not remove endothelium but increased monocyte adherence by 1.46 +/- 0.18-fold (n = 8, P less than 0.05). The proportion of monocytes adhering to veins which had been cultured for 14 days was similar to freshly isolated veins (6.4 +/- 0.8%, n = 7), but in cultured veins, monocytes adhered preferentially to cells with typical endothelial morphology. Endotoxin treatment of cultured freshly-isolated veins increased monocyte adhesion by 1.77 +/- 0.23-fold (n = 8, P less than 0.05). The data show that both endothelial activation, and exposure of subendothelium promote monocyte adhesion to human saphenous vein.
Atherosclerosis 1991 Nov
PMID:Monocyte adhesion to human saphenous vein in vitro. 181 57

The participation of leukocytes in the development of vascular disorders has been observed under various circumstances. Leukocyte activation occurs in extracorporeal blood circulation which lead to a pulmonary vascular sequestration and respiratory distress syndrome. Leukocytes could act on vascular components through at least two different pathways by releasing free oxygen radicals and proteases or by producing mediators such as interleukin 1, Tumor necrosis alpha, leukotrienes. Monocytes macrophages are present in the vascular wall at a very early stage of atherosclerosis. A majority of foam cells have been identified as macrophages loaded with lipids. Lymphocytes and monocytes are present in the atherosclerotic plaque. Leukocytes are also observed in the inflammatory lesion of vasculitis and experimentally activated lymphocytes can induce vasculitis. The molecular bases of leukocyte-endothelium interactions have been determined, and imply specialized molecules. Leukocyte Adhesion Molecule (LeucAM) appear to play a crucial role in leukocyte adhesion. On the endothelial cell side, endothelial cell adhesion molecule, intercellular adhesion molecule are receptors for leukocytes adhesion. They have been recently fully characterized. The better knowledge of leukocyte-vascular wall interactions offers new possible target for therapeutic agents.
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PMID:[Leukocytes and vascular lesions]. 204 28

We studied effects of dietary lipids on some of the initial events in atherogenesis. Adult swine were fed low fat/low cholesterol diets, then challenged with a high cholesterol (1%, w/w) diet supplemented with 11.5% (w/w) butterfat (BF) or MaxEPA fish oil (FO). Serum lipids and monocyte and platelet adhesion to porcine aortic endothelial cells in vitro were measured during feeding of the low fat diet and at 1, 2, and 5 weeks after the dietary challenge. Total cholesterol increased significantly in animals fed the BF and FO diets, but there was no difference between the groups. Animals fed FO had total cholesterol/high-density lipoprotein cholesterol values twice those fed BF (P less than 0.01). After 2 weeks on the hypercholesterolemic diet, monocyte adhesion to endothelial cells increased in swine fed FO by 123% above those fed a low fat diet, and adhesion values remained elevated (56% above baseline value) after 5 weeks. Monocytes from swine fed BF showed increased adhesion by 87, 53, and 14% above those fed the low fat diet at 1, 2, and 5 weeks respectively. Platelet adhesion to endothelial cells decreased (P less than 0.05) after diet change and remained low. Adhesion of platelets from swine fed FO was significantly lower than those fed BF at 1 and cholesterol profile and greater monocyte adhesion to endothelial cells, conditions which in vivo may promote lesion initiation.
Atherosclerosis 1990 Jan
PMID:Effects of dietary fish oil and butterfat on serum lipids and monocyte and platelet interactions with aortic endothelial cells. 217 14

Understanding the mechanisms involved in maintaining the integrity of the vascular endothelium is fundamental to studies on atherosclerosis, thrombosis, inflammation and tumor invasion. One of the essential aspects is the relationship between the endothelial cell (EC) layer and the underlying components of the basement membrane (BM). The importance of the biological role of the individual components of the BM in the promotion of EC adhesion is investigated. In this study suspensions of bovine corneal ECs (BCECs; 5 x 10(4)/ml) were used to investigate the adhesion of EC to collagen type IV and a mixture of fragments of the tetrameric molecule (IV-F, consisting of 75, 120 and 140 kD fragments), as well as collagen types I and III, coated at a 10-micrograms/ml concentration onto glass coverslips in vitro. Adhesion was quantified after 2 h of interaction by direct counting in the light microscope following fixation of the adherent cells. Collagens type IV and IV-F markedly promoted BCEC adhesion both in the presence or absence of 10 or 50% fetal calf serum, indicating that the integrity of the tetrameric molecule is not required for EC adhesion to collagen type IV, but can be replaced by high molecular weight fragments. Collagens type I and III increased EC adhesion in the absence of serum, although not in the presence of serum. Indirect evidence for a possible role of fibronectin in EC adhesion to type-IV collagen is given by the ability of the tetrapeptide (Arg-Gly-Asp-Ser (10 micrograms) to temporarily block (15-30 min) the adhesion-promoting effect of type-IV collagen. The nature of the adhesion sequences on the fragments of type-IV collagen remains to be elucidated.
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PMID:Interaction between endothelial cells and basement membrane components. In vitro studies on endothelial cell adhesion to collagen types I, III, IV and high molecular weight fragments of IV. 253 76

Monocytes and endothelial cell interactions play a key role in the development of vascular lesion, inflammation and atherosclerosis. Leukocyte adhesion is mediated through specific molecules CD11/CD18 complexes on the leukocyte side and the ELAM (Leukocyte Adhesion Molecule) ICAM (Intercellular Adhesion Molecule) on the endothelium cell surface. Several monocyte products damage endothelial cells such as free radicals, oxygen peroxides, proteases, hydrolases, lipases... Various monokines alter endothelial cell function and proliferation. Interleukin 1, gamma interferon, alpha tumor necrosis factor increase ELAM, further more they induce the synthesis of procoagulant activity by endothelial cells. Monocyte derived growth factor stimulates endothelial cells proliferation while transforming growth factors, beta (TGF beta) and TNF alpha inhibit endothelial cell growth. Lipid products of monocyte origins such as leukotrienes induce an activation of endothelial cells which results in a production of prostacyclin. Monocytes may also participate in the coagulation process by producing thromboplastin and coagulation factors and facilitating the tenase (activation of factor X) complex formation. On the other hand, monocyte also synthesize tissue plasminogen activator and inhibitor. The numerous factor produced by monocytes may affect in different ways the endothelial cell behavior.
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PMID:[Monocyte-endothelium relations]. 265 10

Adhesion of leukocytes to the aortic endothelium was studied in specific pathogen-free (SPF) and conventional rats and in SPF rats with diet-induced hypercholesterolemia. Nonspecific esterase activity with alpha-naphthyl acetate as substrate was used to characterize the adhered cells. Phagocytic activity was determined by injecting i.v. 0.1-0.4 ml/100 g doses of Monastral blue B (MbB). Adhesion in SPF rats was 8 +/- 4 esterase (+) cells/mm2. Adhesion in conventional rats was of the same order except in 2 cases with antibodies to Mycoplasma pulmonis and Kilham rat virus, where adhesion was 44 and 68 esterase (+) cells/mm2, respectively. For all MbB doses studied, phagocytic activity arose in a percentage of the adherent cells, ranging from 5 to 85%. Rats fed the hyperlipidic diet for 15 days developed severe hypercholesterolemia and adhesion was drastically increased to 200-700 esterase (+) cells/mm2. Results indicate that: (1) spontaneous pathology in rats may produce an increased adhesion of leukocytes to the endothelium, and (2) phagocytic activity is only expressed in a fraction of the esterase (+) cells adhered to the endothelium.
Atherosclerosis 1989 Jan
PMID:Adhesion of leukocytes to the aortic endothelium of conventional, specific pathogen free (SPF) and hypercholesterolemic SPF rats. 293 Jun 16

Adhesion of bovine endothelial cells on fibronectin and collagen before and after nonenzymatic glycation in vitro has been studied. Nonenzymatic glycation of these proteins reduced their ability to bind endothelial cells. Furthermore, nonenzymatically glycated fibronectin failed to bind to normal and nonenzymatically glycated gelatin and to fibrin. So gelatin and fibrin Sepharoses can be used to separate highly glycated fibronectins from fibronectins with a low degree of nonenzymatic glucose substitution. Sodium dodecylsulfate polyacrylamide gel electrophoresis did not demonstrate a covalent cross-link between nonenzymatically glycated fibronectins. These results present further evidences for the role of nonenzymatic glycation of proteins in the development of vascular complications in long-term diabetes and of atherosclerosis.
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PMID:Diminished adhesion of endothelial aortic cells on fibronectin and collagen layers after nonenzymatic glycation. 340 68


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