MicroRNA-10b Plays a Role in Bone Formation by Suppressing Interleukin-22 in Ankylosing Spondylitis

Objective. The microRNA (miR)-10b is the T helper (Th) 17 cell specific in patients with ankylosing spondylitis (AS). The interleukin (IL)-22, which is closely related to Th17 cells, has been implicated in the regulation of new bone formation in experimental models. Therefore, the aim of this study...

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Published inJournal of rheumatic diseases Vol. 27; no. 1; pp. 61 - 67
Main Authors Pu-reum Park, Sungsin Jo, So-hee Jin, Tae-jong Kim
Format Journal Article
LanguageKorean
Published 대한류마티스학회 01.01.2020
Subjects
Ankylosing spondylitis
MicroRNA
Osteogenesis
Th17 cell
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Summary:Objective. The microRNA (miR)-10b is the T helper (Th) 17 cell specific in patients with ankylosing spondylitis (AS). The interleukin (IL)-22, which is closely related to Th17 cells, has been implicated in the regulation of new bone formation in experimental models. Therefore, the aim of this study was to evaluate whether miR-10b affects bone formation via the IL-22 pathway in AS. Methods. Primary CD4+ T cells from AS were purified and transfected with miR-10b, anti-miR-10b, or scramble. Cell-surface markers and cytokine expression were analyzed by flow cytometry and enzyme-linked immunosorbent assay. Primary bone-derived cells (BdCs) from the facet joints of the spine were isolated, then osteogenic differentiation of primary BdCs was performed. We assessed alkaline phosphatase (ALP) activity and staining of BdCs at early time points. Alizarin red S staining of BdCs was performed at late time points. Results. Overexpression of miR-10b reduced both IL-22 producing cell frequencies and cytokine production in T cells from the patients with AS. The IL-22 significantly increased ALP staining and bone mineralization. The ALP promotor activity of AS-BdCs was notably higher for the IL-22 concentration. The supernatants of the miR-10b overexpression group suppressed ALP activity on osteogenic progenitor cells from the facet joints of the spine in patients with AS. Conclusion. Our data suggest that miR-10b suppresses IL-22 production, which was involved in osteogenic proliferation in AS. Therefore, miR-10b might be a potential therapeutic candidate for regulation of new bone formation in patients with AS. (J Rheum Dis 2020;27:61-67)
Bibliography:The Korean Rheumatism Association
ISSN:2093-940X