Monocyte attachment to activated human vascular endothelium in vitro is mediated by leukocyte adhesion molecule-1 (L-selectin) under nonstatic conditions.

Spertini, Olivier; Luscinskas, Francis W.; Gimbrone, Michael A.; Tedder, Thomas F.

doi:10.1084/jem.175.6.1789

Cited by 140 publications

(91 citation statements)

References 18 publications

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“…Then, 2 ϫ 10 6 T cells were added. After 15 min of incubation at 4°C (or 37°C in some selected experiments) with rotation at 64 rpm on a rocker platform, wells were washed twice with cold PBS and fixed in 1% of glutaraldehyde in PBS (7,8). After overnight fixation, the number of bound T cells was determined by direct counting on an inverted microscope equipped with an ocular micrometer (35).…”

Section: Nonstatic Assays For Evaluation Of T Cell Attachment To Huvementioning

confidence: 99%

“…These experimental models have been employed under either static conditions, to simulate the integrin-mediated adhesion and transmigration, or flow conditions, to reproduce the initial rolling of leukocytes along endothelium (3,6). The in vitro analysis of the different phases of leukocyte rolling, adhesion, and migration has also taken advantage of the different effects of various temperatures on the binding ability of integrins or selectins (7,8).…”

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confidence: 99%

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Salicylates Inhibit T Cell Adhesion on Endothelium Under Nonstatic Conditions: Induction of L-Selectin Shedding by a Tyrosine Kinase-Dependent Mechanism

Gerli

Gresele

Bistoni

et al. 2001

The Journal of Immunology

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Salicylates inhibit T cell adhesion to and transmigration through endothelium by preventing integrin activation induced by contact with endothelial cells. In the present study the effects of aspirin and sodium salicylate on the first steps of T cell adhesion have been analyzed in a nonstatic in vitro system. Salicylates partially reduced adhesion to activated endothelium and, in parallel, L-selectin expression on resting T cells by inducing shedding of the molecule without affecting its mRNA transcript. The role of L-selectin down-regulation in reducing T cell adhesion in this system was supported by the fact that aspirin inhibited T cell adhesion also on plastic-immobilized L-selectin ligand or when α4 integrin-mediated adhesion to endothelium was blocked by specific mAbs. In addition, preincubation of T cells with inhibitors of L-selectin shedding prevented both functional and phenotypic inhibitory effects of salicylates. The decrease in T cell adhesion and L-selectin expression seems to be dependent on intracellular calcium increase and tyrosine kinase activation, because these effects could be reversed by preincubating salicylate-treated T cells with EGTA, genistein, or tyrphostin. Finally, the infusion of aspirin into healthy volunteers induced down-regulation of L-selectin on circulating T cells. These results suggest that salicylates interfere not only with integrin activation, but also with the L-selectin-mediated first steps of T cell binding to endothelium.

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Section: Nonstatic Assays For Evaluation Of T Cell Attachment To Huvementioning

confidence: 99%

mentioning

confidence: 99%

Salicylates Inhibit T Cell Adhesion on Endothelium Under Nonstatic Conditions: Induction of L-Selectin Shedding by a Tyrosine Kinase-Dependent Mechanism

Gerli

Gresele

Bistoni

et al. 2001

The Journal of Immunology

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“…The adhesion assay was performed by adding 1 mL of the concentrated U937 cell suspension to each monolayer under rotating conditions (63 rpm) at 21°C. 28,29 After 10 minutes, nonadhering cells were removed by gentle washing with medium 199, and the monolayers were fixed with 1% paraformaldehyde. The number of adherent cells was determined by counting 6 different fields by using an ocular grid and a 20ϫ objective (0.16 mm 2 /field).…”

Section: Monocytoid Cell Adhesion Assaysmentioning

confidence: 99%

Oleic Acid Inhibits Endothelial Activation

Carluccio¹,

Massaro²,

Bonfrate³

et al. 1999

ATVB

209

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Abstract-Because oleic acid is implicated in the antiatherogenic effects attributed to the Mediterranean diet, we investigated whether this fatty acid can modulate endothelial activation, ie, the concerted expression of gene products involved in leukocyte recruitment and early atherogenesis. We incubated sodium oleate with human umbilical vein endothelial cells for 0 to 72 hours, followed by coincubation of oleate with human recombinant tumor necrosis factor, interleukin (IL)-1␣, IL-1␤, IL-4, Escherichia coli lipopolysaccharide (LPS), or phorbol 12-myristate 13-acetate for a further 6 to 24 hours. The endothelial expression of vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and intercellular adhesion molecule-1 was monitored by cell surface enzyme immunoassays or flow cytometry, and steady-state levels of VCAM-1 mRNA were assessed by Northern blot analysis. At 10 to 100 mol/L for Ͼ24 hours, oleate inhibited the expression of all adhesion molecules tested. After a 72-hour incubation with oleate and a further 16-hour incubation with oleate plus 1 g/mL LPS, VCAM-1 expression was reduced by Ͼ40% compared with control. Adhesion of monocytoid U937 cells to LPS-treated endothelial cells was reduced concomitantly. Oleate also produced a quantitatively similar reduction of VCAM-1 mRNA levels on Northern blot analysis and inhibited nuclear factor-B activation on electrophoretic mobility shift assays. Incubation of endothelial cells with oleate for 72 hours decreased the relative proportions of saturated (palmitic and stearic) acids in total cell lipids and increased the proportions of oleate in total cell lipids without significantly changing the relative proportions of polyunsaturated fatty acids. Although less potent than polyunsaturated fatty acids in inhibiting endothelial activation, oleic acid may contribute to the prevention of atherogenesis through selective displacement of saturated fatty acids in cell membrane phospholipids and a consequent modulation of gene expression for molecules involved in monocyte recruitment. (Arterioscler Thromb Vasc Biol. 1999;19:220-228.)

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“…7 Cytokine-inducible ligands for L-selectin have also been described for peripheral endothelial cells, but their identity is unknown. 8,9 L-selectin-deficient (L-selectin Ϫ/Ϫ ) mice have reduced trauma-and tumor necrosis factor-␣ (TNF-␣)-induced leukocyte rolling, decreased leukocyte recruitment into an inflamed peritoneum, decreased delayed-type hypersensitivity responses, delayed rejection of allogeneic skin transplants, and resistance to lipopolysaccharide (LPS)-induced septic shock. 10 -13 Intercellular adhesion molecule-1 (ICAM-1, CD54) is constitutively expressed at low levels by endothelial cells and is rapidly up-regulated during inflammation, resulting in increased leukocyte-endothelial cell adhesion.…”

mentioning

confidence: 99%

Intercellular Adhesion Molecule-1 and L-Selectin Regulate Bleomycin-Induced Lung Fibrosis

Hamaguchi

Nishizawa

Yasui

et al. 2002

The American Journal of Pathology

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Monocyte attachment to activated human vascular endothelium in vitro is mediated by leukocyte adhesion molecule-1 (L-selectin) under nonstatic conditions.

Cited by 140 publications

References 18 publications

Salicylates Inhibit T Cell Adhesion on Endothelium Under Nonstatic Conditions: Induction of L-Selectin Shedding by a Tyrosine Kinase-Dependent Mechanism

Salicylates Inhibit T Cell Adhesion on Endothelium Under Nonstatic Conditions: Induction of L-Selectin Shedding by a Tyrosine Kinase-Dependent Mechanism

Oleic Acid Inhibits Endothelial Activation

Intercellular Adhesion Molecule-1 and L-Selectin Regulate Bleomycin-Induced Lung Fibrosis

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