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Inhibition of glycogen synthase kinase-3β suppresses inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes and collagen-induced arthritis.

DC FieldValueLanguage
dc.contributor.author권용진-
dc.contributor.author박민찬-
dc.contributor.author박용범-
dc.contributor.author이상원-
dc.contributor.author이수곤-
dc.date.accessioned2015-01-06T16:47:18Z-
dc.date.available2015-01-06T16:47:18Z-
dc.date.issued2014-
dc.identifier.issn1297-319X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/98769-
dc.description.abstractOBJECTIVES: Glycogen synthase kinase (GSK)-3β, a serine/threonine protein kinase, has been implicated as a regulator of the inflammatory response. This study was performed to evaluate the effect of selective GSK-3β inhibitors in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) and collagen-induced arthritis (CIA). METHOD: FLS from RA patients were treated with selective GSK-3β inhibitors, including lithium chloride, 6-bromoindirubin-3'-oxime (BIO), or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8). The effects of GSK-3β inhibition on pro-inflammatory mediators were determined by real-time PCR and ELISA. The levels of NF-κB, phosphorylated JNK, c-jun, ATF-2 and p-38 proteins were evaluated by western blot analysis. The in vivo effects of GSK-3β inhibitors were examined in mice with CIA. RESULTS: Treatment of RA FLS with GSK-3β inhibitors induced dose-dependent reductions in gene expression and the production of pro-inflammatory mediators. The levels of NF-κB, phosphorylated JNK, c-jun, ATF-2 and p-38 were decreased following treatment with GSK-3β inhibitors. GSK-3β inhibitors treatment attenuated clinical and histological severities of CIA in mice. Infiltration of T-cells, macrophages, and tartrate-resistant acid phosphatase positive cells was decreased in joint sections of CIA mice by GSK-3β inhibitors treatment. Serum levels of IL-1β, IL-6, TNF-α and IFN-γ in CIA mice were also significantly decreased in dose-dependent manners by treatment with GSK-3β inhibitors. CONCLUSION: Treatment with GSK-3β inhibitors suppressed inflammatory responses in RA FLS and CIA mice. These findings suggest that the inhibition of GSK-3β can be used as an effective therapeutic agent for RA.-
dc.description.statementOfResponsibilityopen-
dc.format.extent240~246-
dc.relation.isPartOfJoint Bone Spine-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleInhibition of glycogen synthase kinase-3β suppresses inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes and collagen-induced arthritis.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorYong-Jin Kwon-
dc.contributor.googleauthorChong-Hyeon Yoon-
dc.contributor.googleauthorSang-Won Lee-
dc.contributor.googleauthorYong-Beom Park-
dc.contributor.googleauthorSoo-Kon Lee-
dc.contributor.googleauthorMin-Chan Park-
dc.identifier.doi10.1016/j.jbspin.2013.09.006-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00239-
dc.contributor.localIdA01470-
dc.contributor.localIdA01579-
dc.contributor.localIdA02889-
dc.contributor.localIdA02824-
dc.relation.journalcodeJ01216-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S1297319X13002157-
dc.contributor.alternativeNameKwon, Yong Jin-
dc.contributor.alternativeNamePark, Min Chan-
dc.contributor.alternativeNamePark, Yong Beom-
dc.contributor.alternativeNameLee, Sang Won-
dc.contributor.alternativeNameLee, Soo Kon-
dc.contributor.affiliatedAuthorKwon, Yong Jin-
dc.contributor.affiliatedAuthorPark, Min Chan-
dc.contributor.affiliatedAuthorPark, Yong Beom-
dc.contributor.affiliatedAuthorLee, Soo Kon-
dc.contributor.affiliatedAuthorLee, Sang Won-
dc.rights.accessRightsfree-
dc.citation.volume81-
dc.citation.number3-
dc.citation.startPage240-
dc.citation.endPage246-
dc.identifier.bibliographicCitationJoint Bone Spine, Vol.81(3) : 240-246, 2014-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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