Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 황은숙 | * |
dc.date.accessioned | 2016-08-28T12:08:27Z | - |
dc.date.available | 2016-08-28T12:08:27Z | - |
dc.date.issued | 2011 | * |
dc.identifier.issn | 1932-6203 | * |
dc.identifier.other | OAK-7451 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/221517 | - |
dc.description.abstract | Increasing evidence that decreased bone density and increased rates of bone fracture are associated with abnormal metabolic states such as hyperglycemia and insulin resistance indicates that diabetes is a risk factor for osteoporosis. In this study, we observed that TallyHo/JngJ (TH) mice, a polygenic model of type II diabetes, spontaneously developed bone deformities with osteoporotic features. Female and male TH mice significantly gained more body weight than control C57BL/6 mice upon aging. Interestingly, bone density was considerably decreased in male TH mice, which displayed hyperglycemia. The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. Moreover, blockade of IFN-γ further increased RANKL expression and IL-17 production in TH-CD4+ T cells. In addition, the osteoporotic phenotype of TH mice was improved by treatment with alendronate. These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. Accordingly, we propose that TH mice could constitute a beneficial model for osteoporosis. © 2011 Won et al. | * |
dc.language | English | * |
dc.title | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in tallyho/JngJ mice | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 6 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | PLoS ONE | * |
dc.identifier.doi | 10.1371/journal.pone.0018168 | * |
dc.identifier.wosid | WOS:000288813900045 | * |
dc.identifier.scopusid | 2-s2.0-79953034578 | * |
dc.author.google | Won H.Y. | * |
dc.author.google | Lee J.-A. | * |
dc.author.google | Park Z.S. | * |
dc.author.google | Song J.S. | * |
dc.author.google | Kim H.Y. | * |
dc.author.google | Jang S.-M. | * |
dc.author.google | Yoo S.-E. | * |
dc.author.google | Rhee Y. | * |
dc.author.google | Hwang E.S. | * |
dc.author.google | Bae M.A. | * |
dc.contributor.scopusid | 황은숙(8688011100) | * |
dc.date.modifydate | 20240123102458 | * |