ArticleExperimental and therapeutic medicine2023
Expression of long non‑coding RNA NONHSAT227927.1 and its effect on the JAK2/STAT3 signaling pathway and inflammation in patients with ankylosing spondylitis.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Diagnostic value of long noncoding RNAs as biomarkers for Ankylosing Spondylitis: A systematic review and meta-analysis.PloS one · 2025Pooled it
- Jianpi Qingre Tongluo Decoction exerted an anti-inflammatory effect on AS by inhibiting the NONHSAT227927.1/JAK2/STAT3 axis.Heliyon · 2024Article
- Triptolide alleviates the development of inflammation in ankylosing spondylitis via the NONHSAT227927.1/JAK2/STAT3 pathway.Experimental and therapeutic medicine · 2024Article
- A review of long non-coding RNAs in ankylosing spondylitis: pathogenesis, clinical assessment, and therapeutic targets.Frontiers in cell and developmental biology · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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