Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells

Yi Yuan Yang, Chaur Jong Hu, Su Mei Chang, Tzu Yi Tai, Sy Jye Leu

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Atherosclerosis and its complications such as stroke, myocardial infraction and peripheral vascular disease, remain the major causes of morbidity and mortality in the world. Studies have showed that chemokines and adhesion molecules are involved in causing atherosclerosis by promoting directed migration of inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key factors critical for the initiating and developing of atherosclerotic lesions. IL-8, a CXC chemokine, stimulates neutrophil chemotaxis. Aspirin is the most common drug used to prevent the complications of atherosclerosis such as stroke and coronary heart disease. In this study, we found that aspirin inhibited TNF-α (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin at the dose as low as 10 μg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P=0.008) and IL-8 by 26.9% (P=0.0146) as compared to TNF-stimulated release. Antibodies pretreatment were likely to decrease the production of MCP-1 (P

Original languageEnglish
Pages (from-to)207-213
Number of pages7
JournalAtherosclerosis
Volume174
Issue number2
DOIs
Publication statusPublished - Jun 2004
Externally publishedYes

Fingerprint

Chemokine CCL2
Human Umbilical Vein Endothelial Cells
Interleukin-8
Aspirin
Atherosclerosis
Stroke
CXC Chemokines
Peripheral Vascular Diseases
Chemotaxis
Chemokines
Cell Adhesion
Cell Movement
Coronary Disease
Monocytes
Cell Survival
Neutrophils
RNA
Morbidity
Mortality
Antibodies

Keywords

  • Aspirin
  • Atherosclerosis
  • human umbilical vein endothelial cells
  • Human vascular endothelial cell
  • HUVEC
  • IL-8
  • interleukin-8
  • MCP-1
  • Monocyte chemoattractant protein-1
  • monocyte chemoattractant protein-1
  • TNF
  • tumor necrosis factor

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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abstract = "Atherosclerosis and its complications such as stroke, myocardial infraction and peripheral vascular disease, remain the major causes of morbidity and mortality in the world. Studies have showed that chemokines and adhesion molecules are involved in causing atherosclerosis by promoting directed migration of inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key factors critical for the initiating and developing of atherosclerotic lesions. IL-8, a CXC chemokine, stimulates neutrophil chemotaxis. Aspirin is the most common drug used to prevent the complications of atherosclerosis such as stroke and coronary heart disease. In this study, we found that aspirin inhibited TNF-α (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin at the dose as low as 10 μg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1{\%} (P=0.008) and IL-8 by 26.9{\%} (P=0.0146) as compared to TNF-stimulated release. Antibodies pretreatment were likely to decrease the production of MCP-1 (P",
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T1 - Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-α stimulated human umbilical vein endothelial cells

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AU - Hu, Chaur Jong

AU - Chang, Su Mei

AU - Tai, Tzu Yi

AU - Leu, Sy Jye

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