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.