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dc.contributor.author | Murata, Koichi | en |
dc.contributor.author | Yoshitomi, Hiroyuki | en |
dc.contributor.author | Furu, Moritoshi | en |
dc.contributor.author | Ishikawa, Masahiro | en |
dc.contributor.author | Shibuya, Hideyuki | en |
dc.contributor.author | Ito, Hiromu | en |
dc.contributor.author | Matsuda, Shuichi | en |
dc.contributor.alternative | 吉富, 啓之 | ja |
dc.date.accessioned | 2013-12-24T01:42:51Z | - |
dc.date.available | 2013-12-24T01:42:51Z | - |
dc.date.issued | 2014-03 | - |
dc.identifier.issn | 0004-3591 | - |
dc.identifier.uri | http://hdl.handle.net/2433/179622 | - |
dc.description.abstract | Objective. MicroRNAs (miRNAs) are endogenous small noncoding RNAs that regulate the activities of target mRNAs and cellular processes. miR-451 is one of miRNAs conserved perfectly among vertebrates and regulates cell proliferation, invasion, and apoptosis in tumor. However, the role of miR-451 in autoimmune arthritis has been unknown. Our study was designed to identify the role of miR-451 in autoimmune arthritis. Methods. We compared the expression of miR-451 in neutrophils from patients with rheumatoid arthritis (RA) and healthy controls (HCs). The role of miR-451 in neutrophil chemotaxis was evaluated in vivo and in vitro using neutrophils of mice. The regulation of p38 mitogen-activated protein kinase by miR-451 was assessed. Arthritis score and histology in SKG mice were examined by the administration of double-stranded miR-451. Results. miR-451 expression was lower in neutrophils isolated from patients with RA than in those from HCs. Systemic administration of miR-451 significantly disturbed the infiltration of neutrophils in air pouch model without affecting apoptosis of neutrophils. Overexpression of miR-451 significantly suppressed the migration of neutrophils to formyl-methionyl-leucyl-phenylalanine. We identified CPNE3 and Rab5a as direct targets of miR-451. Overexpression of miR-451 suppressed the phosphorylation of p38 mitogen-activated protein kinase (MAPK) via 14-3-3ζ, a known target of miR-451, and Rab5a. In SKG mice, miR-451 treatment reduced the severity of arthritis and the number of infiltrating cells. Conclusions. These results suggest that miR-451 suppresses neutrophil chemotaxis via p38 MAPK and that miR-451 is a potential therapeutic target in the treatment of RA. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | John Wiley & Sons, Inc. | en |
dc.rights | © 2013 American College of Rheumatology. | en |
dc.rights | The definitive version is available at www3.interscience.wiley.com | en |
dc.rights | This is not the published version. Please cite only the published version. | en |
dc.rights | この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 | ja |
dc.title | miR-451 downregulates neutrophil chemotaxis via p38 mitogen-activated protein kinase. | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.ncid | AA00551881 | - |
dc.identifier.jtitle | Arthritis and rheumatism | en |
dc.identifier.volume | 66 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 549 | - |
dc.identifier.epage | 559 | - |
dc.relation.doi | 10.1002/art.38269 | - |
dc.textversion | author | - |
dc.identifier.pmid | 24249046 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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