ArticleBMC musculoskeletal disorders2021
Identification of lncRNAs associated with the pathogenesis of ankylosing spondylitis.
Article in BMC musculoskeletal disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Xinfeng capsule attenuates ankylosing spondylitis by downregulating YTHDC1-mediated mFrontiers in immunology · 2026Article
- Research progress on long non‑coding RNAs in non‑infectious spinal diseases (Review).Molecular medicine reports · 2024Review
- Clinical and genetic factors associated with radiographic damage in patients with ankylosing spondylitis.Annals of the rheumatic diseases · 2023Article
- Novel regulatory role of non-coding RNAs in ankylosing spondylitis.Frontiers in immunology · 2023Review
- Long non-coding RNA RP11-342L8.2, derived from RNA sequencing and validated via RT-qPCR, is upregulated and correlates with disease severity in psoriasis patients.Irish journal of medical science · 2022Article
- The Molecular Mechanism of Long Non-Coding RNA MALAT1-Mediated Regulation of Chondrocyte Pyroptosis in Ankylosing Spondylitis.Molecules and cells · 2022Article
- Screening Key lncRNAs of Ankylosing Spondylitis Using Bioinformatics Analysis.Journal of inflammation research · 2022Article
- Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis.Frontiers in immunology · 2022Review
- RadixBioMed research international · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAnkylosing spondylitis (AS) is a chronic autoimmune disease affecting the sacroiliac joint. To date, few studies have examined the association between long non-coding RNAs (lncRNAs) and AS pathogenesis. As such, we herein sought to characterize patterns of AS-related lncRNA expression and to evaluate the potential role played by these lncRNAs in this complex autoimmune context.
methodsWe conducted a RNA-seq analysis of peripheral blood mononuclear cell (PBMC) samples isolated from five AS patients and corresponding controls. These data were then leveraged to characterize AS-related lncRNA expression patterns. We further conducted GO and KEGG enrichment analyses of the parental genes encoding these lncRNAs, and we confirmed the validity of our RNA-seq data by assessing the expression of six lncRNAs via qRT-PCR in 15 AS and control patient samples. Pearson correlation analyses were additionally employed to examine the associations between the expression levels of these six lncRNAs and patient clinical index values.
resultsWe detected 56,575 total lncRNAs in AS and control patient samples during our initial RNA-seq analysis, of which 200 and 70 were found to be up- and down-regulated (FC > 2 or < 0.05; P < 0.05), respectively, in AS samples relative to controls. In qRT-PCR validation assays, we confirmed the significant upregulation of NONHSAT118801.2, ENST00000444046, and NONHSAT183847.1 and the significant downregulation of NONHSAT205110.1, NONHSAT105444.2, and NONHSAT051856.2 in AS patient samples. We further found the expression of NONHSAT118801.2 and NONHSAT183847.1 to be positively correlated with disease severity.
conclusionOverall, our findings highlight several lncRNAs that are specifically expressed in PBMCs of AS patients, indicating that they may play key functions in the pathogenesis of this autoimmune disease. Specifically, we determined that NONHSAT118801.2 and NONHSAT183847.1 may influence the occurrence and development of AS.
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