Differential regulation of anti-inflammatory proteins in human rheumatoid synoviocyte MH7A cell by celecoxib and ibuprofen = 프로티옴 분석을 통한 관절염 치료제의 기전 규명

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dc.contributor.authorJ H Park-
dc.contributor.authorDong Cho Han-
dc.contributor.authorJina Kim-
dc.contributor.authorS H Hong-
dc.contributor.authorSu-Kyung Lee-
dc.contributor.authorKab Seog Yoon-
dc.contributor.authorJeong-Min Kim-
dc.contributor.authorKwang Hee Son-
dc.contributor.authorK Miyazawa-
dc.contributor.authorByoung-Mog Kwon-
dc.date.accessioned2017-04-19T09:04:19Z-
dc.date.available2017-04-19T09:04:19Z-
dc.date.issued2006-
dc.identifier.issn0024-3205-
dc.identifier.uri10.1016/j.lfs.2005.09.029ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7368-
dc.description.abstractNon-steroidal anti-inflammatory drugs are known to be the most widely used drugs to exert their anti-inflammatory activities. It was examined protein expression profiles of human rheumatoid fibroblast-like synoviocyte MH7A cells treated with celecoxib, a selective cyclooxygenase-2 inhibitor, or ibuprofen, a non-selective cyclooxygenase inhibitor, using two-dimensional gel electrophoresis for comparison the mechanism of the drugs. Altered expression pattern in response to celecoxib is significantly different from that of ibuprofen treated cells. When MH7A cells were treated with celecoxib, 28 proteins were affected at their expression levels. Among them, heat shock proteins (Hsp60 and 70), glucose regulated proteins (Hsp75 and 78) were observed to be up-regulated by 1 to 30 μM concentrations of celecoxib but those proteins were not affected in ibuprofen treated cells. On the other hand, the expression of 19 proteins was changed by ibuprofen and the expression of apolipoprotein E, RNA binding motif 4, CTP-phosphocholine cytidylyltransferase, and phospholipase A2 inhibitory protein was only altered by ibuprofen. The expressions of 15 proteins were affected by both celecoxib and ibuprofen. Our results showed that celecoxib and ibuprofen, though they are known to act as cyclooxygenase inhibitors, could exert a different mode of acting mechanisms in anti-inflammatory processes. The chemical proteomic approach will be useful for figuring out the mode of actions of drugs.-
dc.publisherElsevier-
dc.titleDifferential regulation of anti-inflammatory proteins in human rheumatoid synoviocyte MH7A cell by celecoxib and ibuprofen = 프로티옴 분석을 통한 관절염 치료제의 기전 규명-
dc.title.alternativeDifferential regulation of anti-inflammatory proteins in human rheumatoid synoviocyte MH7A cell by celecoxib and ibuprofen-
dc.typeArticle-
dc.citation.titleLife Sciences-
dc.citation.number19-
dc.citation.endPage2212-
dc.citation.startPage2204-
dc.citation.volume78-
dc.contributor.affiliatedAuthorDong Cho Han-
dc.contributor.affiliatedAuthorJina Kim-
dc.contributor.affiliatedAuthorSu-Kyung Lee-
dc.contributor.affiliatedAuthorKab Seog Yoon-
dc.contributor.affiliatedAuthorJeong-Min Kim-
dc.contributor.affiliatedAuthorKwang Hee Son-
dc.contributor.affiliatedAuthorByoung-Mog Kwon-
dc.contributor.alternativeName박종흠-
dc.contributor.alternativeName한동초-
dc.contributor.alternativeName김진아-
dc.contributor.alternativeName홍수형-
dc.contributor.alternativeName이수경-
dc.contributor.alternativeName윤갑석-
dc.contributor.alternativeName김정민-
dc.contributor.alternativeName손광희-
dc.contributor.alternativeNameMiyazawa-
dc.contributor.alternativeName권병목-
dc.identifier.bibliographicCitationLife Sciences, vol. 78, no. 19, pp. 2204-2212-
dc.identifier.doi10.1016/j.lfs.2005.09.029-
dc.subject.keywordCelecoxib-
dc.subject.keywordCyclooxygenase-
dc.subject.keywordHsps-
dc.subject.keywordIbuprofen-
dc.subject.keywordPhospholipase A2 inhibitory protein-
dc.subject.localcelecoxib-
dc.subject.localCelecoxib-
dc.subject.localCyclooxygenase-
dc.subject.localCyclo-oxygenase-
dc.subject.localCyclooxygenases-
dc.subject.localcyclooxygenase-
dc.subject.localHsps-
dc.subject.localIbuprofen-
dc.subject.localIbuprofen.-
dc.subject.localPhospholipase A2 inhibitory protein-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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