Effect of the H1-Receptor Antagonist Cetirizine on the Stimulated Expression of Adhesion Molecules and the Activation of NFκB in Human Endothelial Cells

2001 ◽  
Vol 124 (1-3) ◽  
pp. 362-364
Author(s):  
Andreas Ambrosch ◽  
Stefan Borgmann ◽  
Jean-Pierre Rihoux ◽  
Wolfgang König
Keyword(s):  
Endothelial Cells ◽  
Receptor Antagonist ◽  
Adhesion Molecules ◽  
Human Endothelial Cells

1P-0187 Effect of humancytomegalovirus and glucose on adhesion molecules expression in cultured human endothelial cells

2003 ◽  
Vol 4 (2) ◽  
pp. 61
Author(s):  
T. Altannvch ◽  
K. Roubalova ◽  
P. Kucera ◽  
M. Andel ◽  
U. Tsetsegmaa
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Human Endothelial Cells

scholarly journals Differential Signal Transduction of Progesterone and Medroxyprogesterone Acetate in Human Endothelial Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (12) ◽  
pp. 5745-5756 ◽  
Author(s):  
Tommaso Simoncini ◽  
Paolo Mannella ◽  
Letizia Fornari ◽  
Antonella Caruso ◽  
Monica Y. Willis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Endothelial Cells ◽  
Glucocorticoid Receptor ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Medroxyprogesterone Acetate ◽  
Intercellular Adhesion Molecule ◽  
Human Endothelial Cells ◽  
Intercellular Adhesion Molecule 1

Abstract The conjugated equine estrogens-only arm of the Women’s Health Initiative trial, showing a trend toward protection from heart disease as opposed to women receiving also medroxyprogesterone acetate (MPA), strengthens the debate on the cardiovascular effects of progestins. We compared the effects of progesterone (P) or MPA on the synthesis of nitric oxide and on the expression of leukocyte adhesion molecules, characterizing the signaling events recruited by these compounds. Although P significantly increases nitric oxide synthesis via transcriptional and nontranscriptional mechanisms, MPA is devoid of such effects. Moreover, when used together with physiological estradiol (E2) concentrations, P potentiates E2 effects, whereas MPA impairs E2 signaling. These findings are observed both in isolated human endothelial cells as well as in vivo, in ovariectomized rat aortas. A marked difference in the recruitment of MAPK and phosphatidylinositol-3 kinase explains the divergent effects of the two gestagens. In addition, both P and MPA decrease the adhesiveness of endothelial cells for leukocytes when given alone or with estrogen. MPA is more potent than P in inhibiting the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. However, when administered together with physiological amounts of glucocorticoids, MPA (which also binds glucocorticoid receptor) markedly interferes with the hydrocortisone-dependent stabilization of the transcription factor nuclear factor κB and with the expression of adhesion molecules, acting as a partial glucocorticoid receptor antagonist. Our findings show significant differences in the signal transduction pathways recruited by P and MPA in endothelial cells, which may have relevant clinical implications.

scholarly journals ICAM-1 Clustering on Endothelial Cells Recruits VCAM-1

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Jaap D. van Buul ◽  
Jos van Rijssel ◽  
Floris P. J. van Alphen ◽  
Anna-Marieke van Stalborch ◽  
Erik P. J. Mul ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Lipid Rafts ◽  
Leukocyte Adhesion ◽  
Transendothelial Migration ◽  
Human Endothelial Cells ◽  
Strong Adhesion ◽  
Integrin Ligands

In the initial stages of transendothelial migration, leukocytes use the endothelial integrin ligands ICAM-1 and VCAM-1 for strong adhesion. Upon adhesion of the leukocyte to endothelial ICAM-1, ICAM-1 is clustered and recruited to the adhered leukocyte, promoting strong adhesion. In this study, we provide evidence for the colocalization of VCAM-1 at sites of ICAM-1 clustering. Anti-ICAM-1 antibody-coated beads were used to selectively cluster and recruit ICAM-1 on primary human endothelial cells. In time, co-localization of ICAM-1 and VCAM-1 around the adherent beads was observed. Biochemical pull-down assays showed that ICAM-1 clustering induced its association to VCAM-1, suggesting a physical link between these two adhesion molecules. The association was partly dependent on lipid rafts as well as on F-actin and promoted adhesion. These data show that VCAM-1 can be recruited, in an integrin-independent fashion, to clustered ICAM-1 which may serve to promote ICAM-1-mediated leukocyte adhesion.

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