scholarly journals Inhibition of Vascular Cell Adhesion Molecule-1 Expression in Human Dermal Microvascular Endothelial Cells by Iron Chelators

2003 ◽  
Vol 121 (5) ◽  
pp. 1229-1230 ◽  
Author(s):  
Thierry Simonart
Blood ◽  
1998 ◽  
Vol 92 (4) ◽  
pp. 1259-1267 ◽  
Author(s):  
Gilles Kaplanski ◽  
Valérie Marin ◽  
Martine Fabrigoule ◽  
Vera Boulay ◽  
Anne-Marie Benoliel ◽  
...  

Thrombin, a central molecule in coagulation, is also involved in inflammation. Notably, thrombin induces endothelial neutrophil adhesion, P- and E-selectin expression, and chemokine production. We show here that thrombin induces expression of intercellular adhesion molecule-1 (ICAM-1; CD54) and vascular cell adhesion molecule-1 (VCAM-1; CD106) on human umbilical vein endothelial cells (HUVECs) associated with increased adhesion of monocytes. Thrombin increased mRNA steady-state levels and expression of ICAM-1 over 24 hours. Thrombin-induced VCAM-1 expression exhibited unusual kinetics, reaching maximum levels after 6 to 12 hours, but decreasing to near baseline after 24 hours. Thrombin activity on HUVECs was mediated through interaction with its specific receptor, because ICAM-1 and VCAM-1 expression were similarly induced by the 14-amino acid thrombin receptor-activating peptide. Thrombin-induced ICAM-1 and VCAM-1 expression was significantly inhibited by hirudin, but not by interleukin-1 receptor antagonist or anti-tumor necrosis factor  monoclonal antibody (MoAb). Thrombin-activated HUVECs significantly increased greater numbers of adhering THP-1 macrophagic cells, peripheral blood mononuclear cells, or purified monocytes than unstimulated HUVECs. This adhesion was inhibited by anti-CD18 and anti-CD49d MoAb, demonstrating that thrombin-induced ICAM-1 and VCAM-1 were functional. These results show that, in addition to selectins, thrombin directly induces a cytokine-independent expression of adhesion molecules of the Ig superfamily on HUVECs that may support firm leukocyte attachment during inflammation. © 1998 by The American Society of Hematology.


1998 ◽  
Vol 82 (8) ◽  
pp. 871-878 ◽  
Author(s):  
Robert E. Gerszten ◽  
Yaw-Chyn Lim ◽  
Han T. Ding ◽  
Karen Snapp ◽  
Geoffrey Kansas ◽  
...  

2013 ◽  
Vol 41 (03) ◽  
pp. 473-485 ◽  
Author(s):  
Gang Hu ◽  
Jiang Liu ◽  
Yong-Zhan Zhen ◽  
Jie Wei ◽  
Yue Qiao ◽  
...  

Reducing the expression of endothelial cell adhesion molecules (ECAMs) is known to decrease inflammation-induced vascular complications. In this study, we explored whether rhein can reduce the inflammation-induced expression of ECAMs in human umbilical vein endothelial cells (HUVECs) with or without lipopolysaccharide (LPS) stimulation. HUVECs were treated with different concentrations of rhein with or without 2.5 μg/ml LPS stimulation. Cell viability was assayed using the MTT method. Real-time PCR and Western blot analysis were used to measure the transcription and expression levels of ECAMs, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-SELECTIN and related signaling proteins. The results indicated that rhein (0–20 μmol/L) and LPS (0–10 μg/ml) had no effect on the viability of HUVECs. LPS could promote the expression of VCAM-1, ICAM-1 and E-SELECTIN. Rhein appeared to target VCAM-1, ICAM-1 and E-SELECTIN, with the transcription and expression of all three factors being reduced by the rhein treatment (10 and 20 μmol/L). The transcription and expression of VCAM-1 were also reduced by treatment with rhein (10 and 20 μmol/L) in the presence of LPS stimulation. In conclusion, rhein treatment reduced the expression of VCAM-1 in HUVECs via a p38-dependent pathway.


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