Cited 32 times in
Inhibition of glycogen synthase kinase-3β suppresses inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes and collagen-induced arthritis.
DC Field | Value | Language |
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dc.contributor.author | 권용진 | - |
dc.contributor.author | 박민찬 | - |
dc.contributor.author | 박용범 | - |
dc.contributor.author | 이상원 | - |
dc.contributor.author | 이수곤 | - |
dc.date.accessioned | 2015-01-06T16:47:18Z | - |
dc.date.available | 2015-01-06T16:47:18Z | - |
dc.date.issued | 2014 | - |
dc.identifier.issn | 1297-319X | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/98769 | - |
dc.description.abstract | OBJECTIVES: 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.statementOfResponsibility | open | - |
dc.format.extent | 240~246 | - |
dc.relation.isPartOf | JOINT BONE SPINE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Antirheumatic Agents/metabolism | - |
dc.subject.MESH | Antirheumatic Agents/pharmacology* | - |
dc.subject.MESH | Antirheumatic Agents/therapeutic use | - |
dc.subject.MESH | Arthritis, Experimental/drug therapy* | - |
dc.subject.MESH | Arthritis, Experimental/metabolism | - |
dc.subject.MESH | Arthritis, Experimental/pathology | - |
dc.subject.MESH | Arthritis, Rheumatoid/drug therapy* | - |
dc.subject.MESH | Arthritis, Rheumatoid/metabolism | - |
dc.subject.MESH | Arthritis, Rheumatoid/pathology | - |
dc.subject.MESH | Cells, Cultured | - |
dc.subject.MESH | Disease Models, Animal | - |
dc.subject.MESH | Fibroblasts/drug effects* | - |
dc.subject.MESH | Glycogen Synthase Kinase 3/antagonists & inhibitors* | - |
dc.subject.MESH | Glycogen Synthase Kinase 3/metabolism | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Inflammation/drug therapy | - |
dc.subject.MESH | Inflammation/metabolism | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Synovial Membrane/drug effects | - |
dc.subject.MESH | Synovial Membrane/pathology* | - |
dc.title | Inhibition of glycogen synthase kinase-3β suppresses inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes and collagen-induced arthritis. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Yong-Jin Kwon | - |
dc.contributor.googleauthor | Chong-Hyeon Yoon | - |
dc.contributor.googleauthor | Sang-Won Lee | - |
dc.contributor.googleauthor | Yong-Beom Park | - |
dc.contributor.googleauthor | Soo-Kon Lee | - |
dc.contributor.googleauthor | Min-Chan Park | - |
dc.identifier.doi | 10.1016/j.jbspin.2013.09.006 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00239 | - |
dc.contributor.localId | A01470 | - |
dc.contributor.localId | A01579 | - |
dc.contributor.localId | A02889 | - |
dc.contributor.localId | A02824 | - |
dc.relation.journalcode | J01216 | - |
dc.identifier.eissn | 1778-7254 | - |
dc.identifier.pmid | 24176738 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S1297319X13002157 | - |
dc.subject.keyword | Collagen-induced arthritis | - |
dc.subject.keyword | Fibroblast-like synoviocytes | - |
dc.subject.keyword | Glycogen synthase kinase-3β | - |
dc.subject.keyword | Rheumatoid arthritis | - |
dc.contributor.alternativeName | Kwon, Yong Jin | - |
dc.contributor.alternativeName | Park, Min Chan | - |
dc.contributor.alternativeName | Park, Yong Beom | - |
dc.contributor.alternativeName | Lee, Sang Won | - |
dc.contributor.alternativeName | Lee, Soo Kon | - |
dc.contributor.affiliatedAuthor | Kwon, Yong Jin | - |
dc.contributor.affiliatedAuthor | Park, Min Chan | - |
dc.contributor.affiliatedAuthor | Park, Yong Beom | - |
dc.contributor.affiliatedAuthor | Lee, Soo Kon | - |
dc.contributor.affiliatedAuthor | Lee, Sang Won | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 81 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 240 | - |
dc.citation.endPage | 246 | - |
dc.identifier.bibliographicCitation | JOINT BONE SPINE, Vol.81(3) : 240-246, 2014 | - |
dc.identifier.rimsid | 38597 | - |
dc.type.rims | ART | - |
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