Abstract
Long non-coding RNAs (lncRNAs) assume pivotal roles in various autoimmune diseases including ankylosing spondylitis (AS). Inflammation affects the progression of multiple diseases. The current research aimed at dissecting out the possible role and mechanism of lncRNAs NONHSAT227927.1 in the pathogenesis of AS. In clinical trials, 50 patients with AS and 30 healthy persons were enrolled, followed by the extraction of peripheral blood mononuclear cells (PBMCs). NONHSAT227927.1 expression was detected using reverse transcription quantitative PCR. Enzyme-linked immunosorbent assay was used to determine the levels of inflammatory cytokines. Human fibroblast-like synoviocytes (FLSs) were induced by PBMC supernatant, after which the activity of FLSs was measured by Cell Counting Kit-8 and the signaling pathway were detected by western blotting. Cell migratory capacity was assessed by Transwell migration assay. NONHSAT227927.1 expression was obviously enhanced in the PBMCs of AS patients. NONHSAT227927.1 expression was positively correlated with immunoglobin A (IgA), erythrocyte sedimentation rate (ESR), complement C3 (C3), visual analog scale, IL-17, and IL-23 Levels but was negatively correlated with IL-10 level. The results of association rules showed that the increase of NONHSAT227927.1 expression was strongly associated with the elevation of IgA, C3, ESR, self-rating anxiety scale and IL-17 levels. Overexpression of NONHSAT227927.1 remarkably augmented the proliferation and migration of AS-PBMCs stimulated by AS-FLSs, facilitated the levels of IL-17 and IL-23, and reduced the IL-10 level. By contrast, NONHSAT227927.1 knockdown decreased cell proliferation and migration and cell viability as well as the levels of IL-17 and IL-23, but increased the level of IL-10. overexpression of NONHSAT227927.1 promoted the phosphorylation of JAK2 and STAT3 proteins, while knockout of NONHSAT227927.1 decreased their phosphorylation. Conclusively, lncRNA NONHSAT227927.1 was overexpressed in AS, which activated the JAK2/STAT3 signaling pathway to upregulate inflammatory factors.