Cited 72 times in
Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice
DC Field | Value | Language |
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dc.contributor.author | 이유미 | - |
dc.date.accessioned | 2014-12-20T17:09:57Z | - |
dc.date.available | 2014-12-20T17:09:57Z | - |
dc.date.issued | 2011 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/94081 | - |
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. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 18168 | - |
dc.relation.isPartOf | PLOS ONE | - |
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 | Alendronate/pharmacology | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Biomarkers/metabolism | - |
dc.subject.MESH | BoneDensity/drug effects | - |
dc.subject.MESH | BoneMarrow/drug effects | - |
dc.subject.MESH | BoneMarrow/metabolism | - |
dc.subject.MESH | BoneResorption/blood | - |
dc.subject.MESH | BoneResorption/metabolism* | - |
dc.subject.MESH | BoneResorption/physiopathology | - |
dc.subject.MESH | CD4-PositiveT-Lymphocytes/drug effects | - |
dc.subject.MESH | CD4-PositiveT-Lymphocytes/metabolism* | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Interferon-gamma/blood | - |
dc.subject.MESH | Interleukin-17/biosynthesis* | - |
dc.subject.MESH | Interleukin-6/blood | - |
dc.subject.MESH | Leptin/blood | - |
dc.subject.MESH | Leptin/pharmacology | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Inbred C57BL | - |
dc.subject.MESH | Osteoblasts/drug effects | - |
dc.subject.MESH | Osteoblasts/metabolism | - |
dc.subject.MESH | Osteoblasts/pathology | - |
dc.subject.MESH | Osteocalcin/blood | - |
dc.subject.MESH | Osteogenesis/drug effects | - |
dc.subject.MESH | RANK Ligand/metabolism* | - |
dc.subject.MESH | Testosterone/pharmacology | - |
dc.title | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Hee Yeon Won | - |
dc.contributor.googleauthor | Jin-Ah Lee | - |
dc.contributor.googleauthor | Zong Sik Park | - |
dc.contributor.googleauthor | Jin Sook Song | - |
dc.contributor.googleauthor | Hee Yun Kim | - |
dc.contributor.googleauthor | Su-Min Jang | - |
dc.contributor.googleauthor | Sung-Eun Yoo | - |
dc.contributor.googleauthor | Youmi Rhee | - |
dc.contributor.googleauthor | Eun Sook Hwang | - |
dc.contributor.googleauthor | Myung Ae Bae | - |
dc.identifier.doi | 10.1371/journal.pone.0018168 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03012 | - |
dc.relation.journalcode | J02540 | - |
dc.identifier.eissn | 1932-6203 | - |
dc.identifier.pmid | 21464945 | - |
dc.contributor.alternativeName | Rhee, Yumie | - |
dc.contributor.affiliatedAuthor | Rhee, Yumie | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 6 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | e18168 | - |
dc.identifier.bibliographicCitation | PLOS ONE, Vol.6(3) : e18168, 2011 | - |
dc.identifier.rimsid | 27224 | - |
dc.type.rims | ART | - |
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