BLOCKADE OF ALPHA1 ADRENERGIC RECEPTOR AMELIORATES INDOXYL SULFATE-INDUCED MONOCYTE CHEMOATTRACTANT PROTEIN-1 EXPRESSION IN HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS BY INHIBITING NADPH OXIDASE- NF-κB PATHWAY

2011 ◽  
Vol 29 ◽  
pp. e336
Author(s):  
T. Morita ◽  
J. Tatebe ◽  
N. Masai ◽  
G. Yoshino ◽  
J. Yamasaki
Keyword(s):  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Adrenergic Receptor ◽  
Umbilical Vein ◽  
Indoxyl Sulfate ◽  
Monocyte Chemoattractant Protein 1 ◽  
Human Umbilical Vein ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Umbilical Vein Endothelial Cells

scholarly journals Reduction of Monocyte Chemoattractant Protein-1 and Interleukin-8 Levels by Ticlopidine in TNF-αStimulated Human Umbilical Vein Endothelial Cells

2009 ◽  
Vol 2009 ◽  
pp. 1-10 ◽  
Author(s):  
Chaur-Jong Hu ◽  
Yueh-Lun Lee ◽  
Neng-Yao Shih ◽  
Yi-Yuan Yang ◽  
Suparat Charoenfuprasert ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Thrombus Formation ◽  
Umbilical Vein ◽  
Interleukin 8 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Human Umbilical Vein ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Treatment And Prevention ◽  
Umbilical Vein Endothelial Cells

Atherosclerosis and its associated complications represent major causes of morbidity and mortality in the industrialized or Western countries. Monocyte chemoattractant protein-1 (MCP-1) is critical for the initiating and developing of atherosclerotic lesions. Interleukin-8 (IL-8), a CXC chemokine, stimulates neutrophil chemotaxis. Ticlopidine is one of the antiplatelet drugs used to prevent thrombus formation relevant to the pathophysiology of atherothrombosis. In this study, we found that ticlopidine dose-dependently decreased the mRNA and protein levels of TNF-α-stimulated MCP-1, IL-8, and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). Ticlopidine declined U937 cells adhesion and chemotaxis as compared to TNF-αstimulated alone. Furthermore, the inhibitory effects were neither due to decreased HUVEC viability, nor through NF-kB inhibition. These results suggest that ticlopidine decreased TNF-αinduced MCP-1, IL-8, and VCAM-1 levels in HUVECs, and monocyte adhesion. Therefore, the data provide additional therapeutic machinery of ticlopidine in treatment and prevention of atherosclerosis.

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