TWEAK promotes osteoclastogenesis in rheumatoid arthritis

Cited 21 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorJ S Park-
dc.contributor.authorS K Kwok-
dc.contributor.authorM A Lim-
dc.contributor.authorH J Oh-
dc.contributor.authorE K Kim-
dc.contributor.authorJ Y Jhun-
dc.contributor.authorJ H Ju-
dc.contributor.authorK S Park-
dc.contributor.authorYoung Woo Park-
dc.contributor.authorS H Park-
dc.contributor.authorH Y Kim-
dc.contributor.authorY G Cho-
dc.contributor.authorM L Cho-
dc.date.accessioned2017-04-19T09:42:44Z-
dc.date.available2017-04-19T09:42:44Z-
dc.date.issued2013-
dc.identifier.issn00029440-
dc.identifier.uri10.1016/j.ajpath.2013.05.027ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11498-
dc.description.abstractBone destruction is critical in the functional disability of patients with rheumatoid arthritis (RA). Osteoclasts, specialized bone-resorbing cells regulated by cytokines, such as receptor activator of NF-κB ligand (RANKL), are primarily implicated in bone destruction in RA. The aim of the study was to examine whether tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor superfamily, has osteoclastogenic activity in patients with RA and in animal models, including mice with collagen-induced arthritis (CIA) and IL-1 receptor antagonist knockout (IL-1RaKO) mice. TWEAK was increased in the synovium, synovial fluid, and serum of patients with RA and in the synovium of CIA mice and IL-1RaKO mice. TWEAK induced RANKL expression in mixed joint cells and splenocytes from CIA mice, IL-1RaKO mice, and fibroblast-like synoviocytes from patients with RA. Both osteoclast precursor cells and osteoclasts express TWEAK receptor fibroblast growth factor-inducible 14. In addition, TWEAK enhanced in vitro osteoclastogenesis without the presence of RANKL-providing cells and by inducing RANKL expression in fibroblast-like synoviocytes. Moreover, treatment with fibroblast growth factor-inducible 14-Fc inhibited RANKL-induced osteoclastogenesis, indicating that endogenous TWEAK also has osteoclastogenic activity. Our data demonstrated that TWEAK promotes osteoclastogenesis in RA, suggesting that therapeutic strategies targeting TWEAK could be effective for treatment of patients with RA, especially in preventing bone destruction.-
dc.publisherElsevier-
dc.titleTWEAK promotes osteoclastogenesis in rheumatoid arthritis-
dc.title.alternativeTWEAK promotes osteoclastogenesis in rheumatoid arthritis-
dc.typeArticle-
dc.citation.titleAmerican Journal of Pathology-
dc.citation.number3-
dc.citation.endPage867-
dc.citation.startPage857-
dc.citation.volume183-
dc.contributor.alternativeName박진실-
dc.contributor.alternativeName곽승기-
dc.contributor.alternativeName임미애-
dc.contributor.alternativeName오혜좌-
dc.contributor.alternativeName김은경-
dc.contributor.alternativeName전주연-
dc.contributor.alternativeName주지현-
dc.contributor.alternativeName박경수-
dc.contributor.alternativeName박영우-
dc.contributor.alternativeName박성환-
dc.contributor.alternativeName김호연-
dc.contributor.alternativeName조영규-
dc.contributor.alternativeName조미라-
dc.identifier.bibliographicCitationAmerican Journal of Pathology, vol. 183, no. 3, pp. 857-867-
dc.identifier.doi10.1016/j.ajpath.2013.05.027-
dc.description.journalClassY-
Appears in Collections:
1. Journal Articles > Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.