Sentences with phrase «endothelial cell adhesion molecule»

The anti-inflammatory actions of platelet endothelial cell adhesion molecule - 1 do not involve regulation of endothelial cell NF - $ ąppa $ B.

In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation.

To determine inducible endothelial cell adhesion molecule expression (E-selectin, VCAM - 1, and ICAM - 1), some of the chambers were given medium containing 10 ng / ml TNF - α for 4 — 6 h (these time points were selected to correlate with the known kinetics of endothelial cell adhesion molecule expression; Refs.

The constitutive and inducible expression of the endothelial cell adhesion molecules E-selectin, ICAM - 1, and VCAM - 1 was assessed by immunohistochemistry (Figs. 4, A — C) ⇓.

The constitutive expression of these endothelial cell adhesion molecules was very similar for most of the lines derived from different organs, i.e., very low expression levels of E-selectin and VCAM - 1 and more pronounced expression of ICAM - 1.

When primary cultures from these mice are stimulated with proinflammatory cytokines, the endothelial cell fraction responds by up - regulating the inducible endothelial cell adhesion molecules, E-selectin and VCAM - 1.

The selection strategy targeted cell populations expressing the inducible endothelial cell adhesion molecules, E-selectin and VCAM - 1, and proved successful in generating microvascular endothelial cell lines from a number of different organs.

Established cell lines exhibited several inherent endothelial properties, including the expression of constitutive and inducible levels of endothelial cell adhesion molecules E-selectin, intercellular adhesion molecule - 1, and vascular cell adhesion molecule - 1, internalization of acetylated low - density lipoprotein, and formation of loop structures on Matrigel surfaces.

The ability to up - regulate endothelial cell adhesion molecules after exposure to cytokines was unaffected by repeated subculturing of cells, because we noted identical staining patterns for passage 30 cells (we did attempt to extend this observation to include later passage cells).

Pilot studies using a variety of strategies suggested that this goal could be best achieved by stimulating primary organ cell cultures with TNF - α (10 ng / ml) and targeting cells expressing the endothelial cell adhesion molecules E-selectin and VCAM - 1 through a FACS - driven strategy.

Not exact matches

We capitalized on one of the innate responses of microvascular endothelial cells, i.e., the up - regulation of cell adhesion molecules in response to inflammatory agents, to generate endothelial cell lines from different organs.

↵ 3 The abbreviations used are: HUVEC, human umbilical vein endothelial cell; DiI - Ac - LDL, 1,1 ′ - dioctadecyl - 3,3,3 ′, 3 ′ - tetramethyl - indocarbocyanine acetylated low - density lipoprotein; FACS, fluorescence - activated cell sorting; FGFR, fibroblast growth factor receptor; Flk, fetal liver kinase; ICAM, intercellular adhesion molecule; mAb, monoclonal antibody; PE, phycoerythrin; TNF, tumor necrosis factor; VCAM, vascular cell adhesion molecule.

However, unlike HUVECs or other commercially available endothelial cell lines, the endothelial cells generated from the H - 2Kb - tsA58 mice retained their ability to mobilize these adhesion molecules despite undergoing numerous population doublings (currently 30 passages).

To stain endothelial cells for adhesion molecules, a peroxidase - conjugated goat antirat IgG F (ab ′) 2 fragment was added for 45 min at room temperature and then removed by washing with PBS.

However, because IFN - γ is widely known to influence several endothelial properties, such as junctional integrity (21) and adhesion molecule expression (22), we elected to remove this cytokine from cultures immediately after the second session of cell selection.

The endothelial cells in insulin - receptor knockout mice expressed more of the VCAM - 1 adhesion molecule that helps white blood cells grab onto the growing plaques, and blood vessels gathered four times as many white blood cells.

Endothelial cell specific adhesion molecule (ESAM) localizes to platelet — platelet contacts and regulates thrombus formation in vivo.

We therefore conducted a cross-sectional analysis to investigate the relations between magnesium intake and plasma concentrations of inflammatory and endothelial biomarkers, including CRP, IL - 6, soluble TNF - α receptor 2 (sTNF - R2), E-selectin, soluble intercellular adhesion molecule 1 (sICAM - 1), and soluble vascular cell adhesion molecule 1 (sVCAM - 1) in apparently healthy women.

Elevated plasma concentrations of soluble forms of endothelial adhesion molecules, released from shedding or proteolytic cleavage from the endothelial cell surface, are considered useful indicators of endothelial dysfunction and activation (20, 25).

A recent in vitro study showed that incorporating a greater extent (2-fold) of TFA in the phospholipid fraction of endothelial cells significantly increased the expression of endothelial adhesion molecules, including ICAM - 1 (25).

Your endothelial cells release nitric oxide, von Willebrand factors, and adhesion molecules, which all contribute to vascular homeostasis

Resveratrol has been found to inhibit the expression of adhesion molecules in cultured endothelial cells (43, 44).