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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
박예수
Keywords
Interleukin-32; Osteoblast differentiation; Ankylosing spondylitis
Issue Date
2015-12
Publisher
BIOMED CENTRAL LTD
Citation
ARTHRITIS RESEARCH & THERAPY, v. 17, Page. 350-358
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
http://www.arthritis-research.com/content/17/1/350http://hdl.handle.net/20.500.11754/29493
ISSN
1478-6354; 1478-6362
DOI
10.1186/s13075-015-0870-4
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COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
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