4.6 Article

LncRNA MEG3 inhibits the inflammatory response of ankylosing spondylitis by targeting miR-146a

Journal

MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 466, Issue 1-2, Pages 17-24

Publisher

SPRINGER
DOI: 10.1007/s11010-019-03681-x

Keywords

Ankylosing spondylitis; MEG3; miR-146a; Inflammatory response; Cytokines

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Ankylosing spondylitis (AS) is a progressive systemic disease characterized by chronic inflammation response of the sacroiliac joint and spine. Long non-coding RNAs (lncRNAs) are widely involved in the regulation of various diseases. However, the role of lncRNA maternally expressed gene 3 (MEG3) in the inflammatory response of AS has not been studied. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory cytokines interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in tissues and cells. The expression levels of MEG3, microRNA-146a (miR-146a), and inflammatory cytokines were measured by quantitative real-time PCR (qRT-PCR). Correlation between MEG3 or miR-146a and inflammatory cytokines was analyzed by Pearson analysis. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to clarify the interaction between MEG3 and miR-146a. MEG3 was downregulated in AS patients, negatively correlated with the levels of IL-1 beta, IL-6, and TNF-alpha, and blocked the inflammatory response of AS. MiR-146a was upregulated in AS patients and could interact with MEG3. The expression of miR-146a was positively correlated with IL-1 beta, IL-6, and TNF-alpha levels. Overexpression of miR-146a reversed the inhibitory effect of abnormal MEG3 expression on inflammatory cytokines. LncRNA MEG3 plays an anti-inflammatory role in AS partially through targeting miR-146a, which provides a potential new means for the treatment of AS patients.

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