DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jung, Y | ko |
dc.contributor.author | Song, S | ko |
dc.contributor.author | Choi, Chulhee | ko |
dc.date.accessioned | 2013-03-07T13:23:37Z | - |
dc.date.available | 2013-03-07T13:23:37Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2008-04 | - |
dc.identifier.citation | IMMUNOLOGY LETTERS, v.117, pp.63 - 69 | - |
dc.identifier.issn | 0165-2478 | - |
dc.identifier.uri | http://hdl.handle.net/10203/90277 | - |
dc.description.abstract | In this study, we investigated the anti-inflammatory effect of various peroxisome proliferator activated receptor gamma (PPAR gamma) agonists (15-deoxy-Delta 12,14-prostaglandin J(2), troglitazone, rosiglitazone, ciglitazone) on human aortic endothelial cells. Pretreatment with PPAR gamma agonists abrogated tumor necrosis factor alpha (TNF alpha)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and subsequent monocytic adhesion by endothelial cells. Because reactive oxygen species (ROS) have been reported to play important roles in pro-inflammatory signal transduction, the involvement of ROS was investigated as a potential mechanism of anti-inflammatory effect of PPAR gamma ligands. Consistent with previous reports in other cell types, blockade of TNF alpha-induced ROS by treatment with N-acetylcysteine, diphertylene iodonium or NADPH oxidase 4 (NOX4) siRNA suppressed TNF alpha-induced ICAM-1 expression and subsequent monocytic adhesion, indicating that TNF alpha mediates pro-inflammatory signals via NOX4-dependent ROS generation in human endothelial cells. Finally, pretreatment with PPAR gamma agonists significantly suppressed TNF alpha-induced increases of intracellular ROS. Our results collectively suggest that PPAR gamma agonists might exert an anti-inflammatory effect on endothelial cells in a ROS-dependent manner. (C) 2007 Elsevier B.V. All rights reserved. | - |
dc.language | English | - |
dc.publisher | ELSEVIER SCIENCE BV | - |
dc.subject | TUMOR-NECROSIS-FACTOR | - |
dc.subject | SMOOTH-MUSCLE-CELLS | - |
dc.subject | NAD(P)H OXIDASE | - |
dc.subject | PPAR-GAMMA | - |
dc.subject | CARDIOVASCULAR BIOLOGY | - |
dc.subject | INFLAMMATORY RESPONSES | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | KAPPA-B | - |
dc.subject | ANGIOTENSIN | - |
dc.subject | DISEASE | - |
dc.title | Peroxisome proliferator activated receptor gamma agonists suppress TNF alpha-induced ICAM-1 expression by endothelial cells in a manner potentially dependent on inhibition of reactive oxygen species | - |
dc.type | Article | - |
dc.identifier.wosid | 000255183400009 | - |
dc.identifier.scopusid | 2-s2.0-40649104327 | - |
dc.type.rims | ART | - |
dc.citation.volume | 117 | - |
dc.citation.beginningpage | 63 | - |
dc.citation.endingpage | 69 | - |
dc.citation.publicationname | IMMUNOLOGY LETTERS | - |
dc.identifier.doi | 10.1016/j.imlet.2007.12.002 | - |
dc.contributor.localauthor | Choi, Chulhee | - |
dc.contributor.nonIdAuthor | Jung, Y | - |
dc.contributor.nonIdAuthor | Song, S | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | peroxisome proliferator activated receptor gamma | - |
dc.subject.keywordAuthor | tumor necrosis factor alpha | - |
dc.subject.keywordAuthor | intercellular adhesion molecule-1 | - |
dc.subject.keywordAuthor | reactive oxygen species | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordPlus | TUMOR-NECROSIS-FACTOR | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE-CELLS | - |
dc.subject.keywordPlus | NAD(P)H OXIDASE | - |
dc.subject.keywordPlus | PPAR-GAMMA | - |
dc.subject.keywordPlus | CARDIOVASCULAR BIOLOGY | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSES | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | KAPPA-B | - |
dc.subject.keywordPlus | ANGIOTENSIN | - |
dc.subject.keywordPlus | DISEASE | - |
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