Linked Life Data

20573493

Source:http://linkedlifedata.com/resource/pubmed/id/20573493

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-17
pubmed:abstractText
This study was conducted to test the hypothesis that n-3 polyunsaturated fatty acids are able to down-regulate expression of adhesion molecules and nuclear factor-?B (NF-?B) activation in vascular endothelial cells, in addition to reducing atherosclerotic lesions in vivo. We report here that docosahexaenoic acid (DHA) reduces atherosclerotic lesions in the aortic arteries of apolipoprotein E knockout (apoE(-/-)) mice. Consistent with the observation in animal study, DHA inhibited THP-1 cell adhesion to tumor necrosis factor ? (TNF-?)-activated human aortic endothelial cells (HAECs). Expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) on the cell surface of HAECs was determined by cell-surface enzyme-linked immunosorbent assay. DHA and eicosapentaenoic acid decreased VCAM-1 expression in a dose-dependent manner in TNF-? treated HAECs, while cis-linoleic acid and arachidonic acid did not have any significant effect on either VCAM-1 or ICAM-1 expression. Moreover, DHA significantly reduced VCAM-1 protein expression in the cell lysates of TNF-?-treated HAECs, as determined by Western blot analysis. In line with NF-?B signaling pathway, DHA suppressed the TNF-?-activated I?B? phosphorylation and degradation as well as I?B kinase-? phosphorylation. Subsequently, translocation of the NF-?B (p50/p65) and AP-1 (c-Fos/c-Jun) subunits was down-regulated by DHA in the nucleus of HAECs. These results suggest that DHA negatively regulates TNF-?-induced VCAM-1 expression through attenuation of NF-?B signaling pathway and AP-1 activation. This study provides evidence that DHA may contribute to the prevention of atherosclerosis and inflammatory diseases in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1873-4847
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
187-94
pubmed:meshHeading
pubmed-meshheading:20573493-Animals, pubmed-meshheading:20573493-Aorta, pubmed-meshheading:20573493-Cell Line, pubmed-meshheading:20573493-Docosahexaenoic Acids, pubmed-meshheading:20573493-Down-Regulation, pubmed-meshheading:20573493-Endothelial Cells, pubmed-meshheading:20573493-Endothelium, Vascular, pubmed-meshheading:20573493-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:20573493-Humans, pubmed-meshheading:20573493-I-kappa B Kinase, pubmed-meshheading:20573493-I-kappa B Proteins, pubmed-meshheading:20573493-Intercellular Adhesion Molecule-1, pubmed-meshheading:20573493-Male, pubmed-meshheading:20573493-Mice, pubmed-meshheading:20573493-Mice, Knockout, pubmed-meshheading:20573493-NF-kappa B, pubmed-meshheading:20573493-Phosphorylation, pubmed-meshheading:20573493-Random Allocation, pubmed-meshheading:20573493-Signal Transduction, pubmed-meshheading:20573493-Transcription Factor AP-1, pubmed-meshheading:20573493-Tumor Necrosis Factor-alpha, pubmed-meshheading:20573493-Vascular Cell Adhesion Molecule-1
pubmed:year
2011
pubmed:articleTitle
Docosahexaenoic acid attenuates VCAM-1 expression and NF-?B activation in TNF-?-treated human aortic endothelial cells.
pubmed:affiliation
Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 112, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't