High level of interleukin-32 gamma in the joint of ankylosing spondylitis is associated with osteoblast differentiation
- Title
- High level of interleukin-32 gamma in the joint of ankylosing spondylitis is associated with osteoblast differentiation
- Author
- 김태환
- Keywords
- Interleukin-32; Osteoblast differentiation; Ankylosing spondylitis
- Issue Date
- 2015-12
- Publisher
- BIOMED CENTRAL LTD
- Citation
- ARTHRITIS RESEARCH & THERAPY, v. 17, NO 350, Page. 35-43
- Abstract
- Backgound: The formation of bony spurs and ankylosis is a key pathognomic feature in ankylosing spondylitis (AS) and results in functional impairment. The aim of this study was to investigate the role of IL-32 gamma in osteoblast (OB) differentiation and its association with the pathogenesis of AS. Methods: The concentration and expression of IL-32 gamma were evaluated in synovial fluid and tissue from patients with AS, rheumatoid arthritis (RA) and osteoarthritis (OA), using enzyme-linked immunosorbent assay and immunohistochemistry. To establish whether IL-32 gamma affects OB differentiation, we used calvarial cells of IL-32 gamma transgenic (TG) mice or wild-type (WT) mice. To elucidate the mechanism of osteoblastogenesis, levels of regulators were assayed in IL-32 gamma TG mice and in primary OBs after IL-32 gamma stimulation. Results: The IL-32 gamma levels were higher in the synovial fluid of AS patients compared with RA or OA patients and the expression of IL-32 was higher in AS synovia than in RA or OA synovia. Additional IL-32 gamma stimulation in precursor cells enhanced OB differentiation potentially and IL-32 gamma TG mice showed higher rates of OB differentiation than WT mice. IL-32 gamma reduced the expression of DKK-1, a negative regulator, in both WT precursor cells and human OBs and the constitutive expression of DKK-1 was suppressed in calvarial cells from IL-32 gamma TG mice. Conclusions: The elevated level of IL-32 gamma in AS joint could enhance OB differentiation via DKK-1 suppression. Therefore, IL-32 gamma might be a putative molecular target to prevent the abnormal bone formation in AS.
- URI
- https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-015-0870-4http://hdl.handle.net/20.500.11754/30053
- ISSN
- 1478-6354; 1478-6362
- DOI
- 10.1186/s13075-015-0870-4
- Appears in Collections:
- COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
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