Araki Kei, Mokuda Sho, Kohno Hiroki, Oka Naoya, Watanabe Hirofumi, Ishitoku Michinori, Sugimoto Tomohiro, Yoshida Yusuke, Masumoto Junya, Hirata Shintaro
Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, 734- 8551, Japan.
Division of Laboratory Medicine, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Sci Rep. 2025 Jun 3;15(1):19416. doi: 10.1038/s41598-025-02840-z.
Fibroblast-like synoviocytes (FLS) contribute significantly to the pathogenesis of rheumatoid arthritis (RA), particularly through their roles in synovitis and joint destruction. The microRNAs (miRNAs) are short non-coding RNA that regulate gene expression post-transcriptionally. Although more than 2000 human miRNAs are registered, comprehensive analyses of miRNA expression in FLS are limited. Herein, we investigated the relationship between miRNAs and FLS. Next-generation sequencing (small RNA-seq) was performed on primary cultured FLS derived from patients with RA to analyze the mature miRNA expression pattern. To assess inflammation-induced changes in miRNA levels, FLS were cultured with cytokines and evaluated by RT-qPCR. MiRNA mimics were transfected into FLS and an immortalized synovial fibroblast cell line (MH7A cells), and validated using conventional RNA-seq. Out of 2861 mature miRNAs, 297 mature miRNAs were detected and intronic miRNAs were predominated. Notably, hsa-miR-21-5p was abundantly expressed and its expression was enhanced by IL-6 stimulation. The induction of miR-21-5p mimic decreased the expression of Programmed Cell Death 4 (PDCD4) and Osteoprotegerin (OPG), while upregulating Semaphorin 5A (SEMA5A). MiR-21-5p mimic led to enhanced cell proliferation. These data suggest that hsa-miR-21-5p in FLS may exacerbate the pathophysiology of rheumatoid synovitis by promoting FLS proliferation, highlighting its potential as a therapeutic target in RA.
成纤维样滑膜细胞(FLS)在类风湿关节炎(RA)的发病机制中起重要作用,尤其是通过它们在滑膜炎和关节破坏中的作用。微小RNA(miRNA)是短的非编码RNA,可在转录后调节基因表达。尽管已注册了2000多种人类miRNA,但对FLS中miRNA表达的全面分析仍然有限。在此,我们研究了miRNA与FLS之间的关系。对来自RA患者的原代培养FLS进行了下一代测序(小RNA测序),以分析成熟miRNA的表达模式。为了评估炎症诱导的miRNA水平变化,将FLS与细胞因子一起培养并通过RT-qPCR进行评估。将miRNA模拟物转染到FLS和永生化滑膜成纤维细胞系(MH7A细胞)中,并使用常规RNA测序进行验证。在2861种成熟miRNA中,检测到297种成熟miRNA,且内含子miRNA占主导。值得注意的是,hsa-miR-21-5p大量表达,其表达受到IL-6刺激的增强。miR-21-5p模拟物的诱导降低了程序性细胞死亡4(PDCD4)和骨保护素(OPG)的表达,同时上调了信号素5A(SEMA5A)。miR-21-5p模拟物导致细胞增殖增强。这些数据表明,FLS中的hsa-miR-21-5p可能通过促进FLS增殖而加剧类风湿滑膜炎的病理生理,突出了其作为RA治疗靶点的潜力。