Abstract

Background: Atherosclerosis potentially represents a chronic inflammatory disease in which both endothelial cells and monocytes are involved. Monocyte-endothelium adhesion, which is heavily dependent on the expression of adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1), is one of the key stages of atherogenesis. Toll-like receptor 4 (TLR4) has been found in atheroma and adventitia of human atherosclerotic coronary arteries. In TLR4-knockout mice studies, TLR4 contributes to atherogenesis via the nuclear factor-kappa B signal pathway, a process within which adhesion molecules are involved. Bacterial infection, such as Chlamydia pneumonia and lipopolysaccharide (LPS), is well known to act as the ligand of TLR4, triggering the overexpression of adhesion molecules and other inflammatory mediators, which can ultimately lead to atherogenesis. Purpose: In this study, we explore the role of TLR4 in the monocyte-endothelium adhesion. Method: The monocyte-endothelium adhesion triggered by LPS on human coronary artery endothelial cells was tested by anti-TLR4 antibody and anti-VCAM-1 antibody. Results: The inhibition of TLR4 could suppress the overexpression of VCAM-1 in messenger RNA and protein levels. Both anti-TLR4 antibody and anti-VCAM-1 antibody interfere with monocyte-endothelium adhesion. Conclusion: We conclude that LPS upregulates VCAM-1 by interacting with TLR4 and then enhances monocyte-endothelium adhesion. These findings may imply that the inhibition of TLR4 could be a potential target for atherosclerosis therapy.

Original languageEnglish
Pages (from-to)297-301
Number of pages5
JournalJournal of Experimental and Clinical Medicine(Taiwan)
Volume2
Issue number6
DOIs
Publication statusPublished - Dec 2010

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Toll-Like Receptor 4
Vascular Cell Adhesion Molecule-1
Endothelium
Lipopolysaccharides
Monocytes
Atherosclerosis
Anti-Idiotypic Antibodies
Coronary Vessels
Endothelial Cells
Chlamydophila pneumoniae
Adventitia
Antibodies
NF-kappa B
Atherosclerotic Plaques
Bacterial Infections
Knockout Mice
Signal Transduction
Chronic Disease
Up-Regulation
Ligands

Keywords

  • Atherosclerosis
  • Lipopolysaccharide
  • Monocyte-endothelium adhesion
  • Toll-like receptor 4
  • VCAM-1

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Toll-like Receptor 4 and Vascular Cell Adhesion Molecule 1 in Monocyte-Endothelium Adhesion Induced by Lipopolysaccharide",
abstract = "Background: Atherosclerosis potentially represents a chronic inflammatory disease in which both endothelial cells and monocytes are involved. Monocyte-endothelium adhesion, which is heavily dependent on the expression of adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1), is one of the key stages of atherogenesis. Toll-like receptor 4 (TLR4) has been found in atheroma and adventitia of human atherosclerotic coronary arteries. In TLR4-knockout mice studies, TLR4 contributes to atherogenesis via the nuclear factor-kappa B signal pathway, a process within which adhesion molecules are involved. Bacterial infection, such as Chlamydia pneumonia and lipopolysaccharide (LPS), is well known to act as the ligand of TLR4, triggering the overexpression of adhesion molecules and other inflammatory mediators, which can ultimately lead to atherogenesis. Purpose: In this study, we explore the role of TLR4 in the monocyte-endothelium adhesion. Method: The monocyte-endothelium adhesion triggered by LPS on human coronary artery endothelial cells was tested by anti-TLR4 antibody and anti-VCAM-1 antibody. Results: The inhibition of TLR4 could suppress the overexpression of VCAM-1 in messenger RNA and protein levels. Both anti-TLR4 antibody and anti-VCAM-1 antibody interfere with monocyte-endothelium adhesion. Conclusion: We conclude that LPS upregulates VCAM-1 by interacting with TLR4 and then enhances monocyte-endothelium adhesion. These findings may imply that the inhibition of TLR4 could be a potential target for atherosclerosis therapy.",
keywords = "Atherosclerosis, Lipopolysaccharide, Monocyte-endothelium adhesion, Toll-like receptor 4, VCAM-1",
author = "Hung, {Chia Hsiu} and Dean Wu and Lin, {Feng Yen} and Yuan, {Rey Yue} and Hu, {Chaur Jong}",
year = "2010",
month = "12",
doi = "10.1016/j.jecm.2010.10.003",
language = "English",
volume = "2",
pages = "297--301",
journal = "Journal of Experimental and Clinical Medicine",
issn = "1878-3317",
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T1 - Toll-like Receptor 4 and Vascular Cell Adhesion Molecule 1 in Monocyte-Endothelium Adhesion Induced by Lipopolysaccharide

AU - Hung, Chia Hsiu

AU - Wu, Dean

AU - Lin, Feng Yen

AU - Yuan, Rey Yue

AU - Hu, Chaur Jong

PY - 2010/12

Y1 - 2010/12

N2 - Background: Atherosclerosis potentially represents a chronic inflammatory disease in which both endothelial cells and monocytes are involved. Monocyte-endothelium adhesion, which is heavily dependent on the expression of adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1), is one of the key stages of atherogenesis. Toll-like receptor 4 (TLR4) has been found in atheroma and adventitia of human atherosclerotic coronary arteries. In TLR4-knockout mice studies, TLR4 contributes to atherogenesis via the nuclear factor-kappa B signal pathway, a process within which adhesion molecules are involved. Bacterial infection, such as Chlamydia pneumonia and lipopolysaccharide (LPS), is well known to act as the ligand of TLR4, triggering the overexpression of adhesion molecules and other inflammatory mediators, which can ultimately lead to atherogenesis. Purpose: In this study, we explore the role of TLR4 in the monocyte-endothelium adhesion. Method: The monocyte-endothelium adhesion triggered by LPS on human coronary artery endothelial cells was tested by anti-TLR4 antibody and anti-VCAM-1 antibody. Results: The inhibition of TLR4 could suppress the overexpression of VCAM-1 in messenger RNA and protein levels. Both anti-TLR4 antibody and anti-VCAM-1 antibody interfere with monocyte-endothelium adhesion. Conclusion: We conclude that LPS upregulates VCAM-1 by interacting with TLR4 and then enhances monocyte-endothelium adhesion. These findings may imply that the inhibition of TLR4 could be a potential target for atherosclerosis therapy.

AB - Background: Atherosclerosis potentially represents a chronic inflammatory disease in which both endothelial cells and monocytes are involved. Monocyte-endothelium adhesion, which is heavily dependent on the expression of adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1), is one of the key stages of atherogenesis. Toll-like receptor 4 (TLR4) has been found in atheroma and adventitia of human atherosclerotic coronary arteries. In TLR4-knockout mice studies, TLR4 contributes to atherogenesis via the nuclear factor-kappa B signal pathway, a process within which adhesion molecules are involved. Bacterial infection, such as Chlamydia pneumonia and lipopolysaccharide (LPS), is well known to act as the ligand of TLR4, triggering the overexpression of adhesion molecules and other inflammatory mediators, which can ultimately lead to atherogenesis. Purpose: In this study, we explore the role of TLR4 in the monocyte-endothelium adhesion. Method: The monocyte-endothelium adhesion triggered by LPS on human coronary artery endothelial cells was tested by anti-TLR4 antibody and anti-VCAM-1 antibody. Results: The inhibition of TLR4 could suppress the overexpression of VCAM-1 in messenger RNA and protein levels. Both anti-TLR4 antibody and anti-VCAM-1 antibody interfere with monocyte-endothelium adhesion. Conclusion: We conclude that LPS upregulates VCAM-1 by interacting with TLR4 and then enhances monocyte-endothelium adhesion. These findings may imply that the inhibition of TLR4 could be a potential target for atherosclerosis therapy.

KW - Atherosclerosis

KW - Lipopolysaccharide

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