LncRNA HOTTIP impacts the proliferation and differentiation of fibroblast-like synoviocytes in ankylosing spondylitis through the microRNA-30b-3p/PGK1 axis

Li, Wei; Zhang, Xin; Yao, Yu; Zheng, Weizhuo; Tian, Jie

doi:10.1186/s13018-023-03653-4

Cited by 3 publications

(2 citation statements)

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“…HOTTIP has been implicated in the pathogenesis of osteosarcoma, endochondral ossification, and osteoarthritic progression ( Kim et al, 2013 ; Li et al, 2015 ). In an experiment conducted by Wei L et al, elevated levels of HOTTIP were detected, while miR-30b-3p was reduced in AS synovial tissues and AS fibroblast-like synoviocytes (ASFLSs) in mouse models ( Wei et al, 2023 ). The study further suggested that overexpressed miR-30b-3p or inhibited HOTTIP hindered the proliferation and differentiation of ASFLSs by suppressing phosphoglycerate kinase 1(PGK1), thereby restraining AS development.…”

Section: Lncrnas Involved In the Pathogenesis Of Asmentioning

confidence: 99%

A review of long non-coding RNAs in ankylosing spondylitis: pathogenesis, clinical assessment, and therapeutic targets

Wang,

Yang,

et al. 2024

Front. Cell Dev. Biol.

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Ankylosing spondylitis (AS) is a chronic immune-mediated type of inflammatory arthritis characterized by inflammation, bone erosion, and stiffness of the spine and sacroiliac joints. Despite great efforts put into the investigation of the disease, the pathogenesis of AS remains unclear, posing challenges in identifying ideal targets for diagnosis and treatment. To enhance our understanding of AS, an increasing number of studies have been conducted. Some of these studies reveal that long non-coding RNAs (lncRNAs) play crucial roles in the etiology of AS. Some certain lncRNAs influence the development of AS by regulating inflammatory responses, autophagy, apoptosis, and adipogenesis, as well as the proliferation and differentiation of cells. Additionally, some lncRNAs demonstrate potential as biomarkers, aiding in monitoring disease progression and predicting prognosis. In this review, we summarize recent studies concerning lncRNAs in AS to elucidate the underlying mechanisms in which lncRNAs are involved and their potential values as biomarkers for disease assessment and druggable targets for therapy.

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Section: Lncrnas Involved In the Pathogenesis Of Asmentioning

confidence: 99%

A review of long non-coding RNAs in ankylosing spondylitis: pathogenesis, clinical assessment, and therapeutic targets

Wang,

Yang,

et al. 2024

Front. Cell Dev. Biol.

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“…For example, lncRNA NKILA affects plasma TGF-β1 level [ 25 ], and lncRNA H19 mediates the release of inflammatory cytokines IL-17/IL-23 in AS [ 26 ]. Down-regulating lncRNA HOTTIP improves AS progression by inhibiting the proliferation and differentiation of fibroblast-like synovial cells [ 27 ]. Wang et al [ 28 ] have demonstrated that lncRNA HULC promotes inflammatory responses in cholangiocarcinoma by affecting the production of IL-6.…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of long noncoding RNA HULC inhibits the inflammatory response in ankylosing spondylitis by reducing miR-556-5p-mediated YAP1 expression

Yi,

Song,

Liu

et al. 2023

J Orthop Surg Res

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Objective Ankylosing spondylitis (AS) is a progressive systemic disease characterized by a chronic inflammatory response in the sacroiliac joints and spine. Long noncoding RNAs suggest significant actions in the progression of AS. Therefore, a specific lncRNA, highly upregulated in liver cancer (HULC), was studied here regarding its functions and related mechanisms in AS. Methods Measurements of miR-556-5p, HULC, and YAP1 expression were performed on AS cartilage tissues and chondrocytes. The interaction between miR-556-5p and HULC or YAP1 was verified. CCK-8, flow cytometry and enzyme-linked immunosorbent assay were used to evaluate the effects of HULC, miR-556-5p, and YAP1 on the proliferation, apoptosis, and inflammatory response of AS chondrocytes. Furthermore, the action of HULC/miR-556-5p/YAP1 was experimentally observed in AS mice. Results HULC and YAP1 levels were augmented, while miR-556-5p levels were suppressed in AS cartilage tissues and chondrocytes. Downregulating HULC or upregulating miR-556-5p stimulated chondrocyte proliferation and inhibited apoptosis and inflammation in AS. miR-556-5p was a downstream factor of HULC, and YAP1 was a potential target of miR-556-5p. The improvement effect of downregulated HULC on AS chondrocytes was saved when YAP1 expression was forced. In addition, silence of HULC improved the pathological injury of spinal cartilage in AS mice by enhancing miR-556-5p-related regulation of YAP1. Conclusion HULC inhibition relieves the inflammatory response in AS by reducing miR-556-5p-mediated YAP1 expression.

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Proteomic and genomic profiling of plasma exosomes from patients with ankylosing spondylitis

et al. 2023

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IntroductionRecent advances in understanding the biology of ankylosing spondylitis (AS) using innovative genomic and proteomic approaches offer the opportunity to address current challenges in AS diagnosis and management. Altered expression of genes, microRNAs (miRNAs) or proteins may contribute to immune dysregulation and may play a significant role in the onset and persistence of inflammation in AS. The ability of exosomes to transport miRNAs across cells and alter the phenotype of recipient cells has implicated exosomes in perpetuating inflammation in AS. This study reports the first proteomic and miRNA profiling of plasma-derived exosomes in AS using comprehensive computational biology analysis.MethodsPlasma samples from patients with AS and healthy controls (HC) were isolated via ultracentrifugation and subjected to extracellular vesicle flow cytometry analysis to characterise exosome surface markers by a multiplex immunocapture assay. Cytokine profiling of plasma-derived exosomes and cell culture supernatants was performed. Next-generation sequencing was used to identify miRNA populations in exosomes enriched from plasma fractions. CD4+ T cells were sorted, and the frequency and proliferation of CD4+ T-cell subsets were analysed after treatment with AS-exosomes using flow cytometry.ResultsThe expression of exosome marker proteins CD63 and CD81 was elevated in the patients with AS compared with HC (q<0.05). Cytokine profiling in plasma-derived AS-exosomes demonstrated downregulation of interleukin (IL)-8 and IL-10 (q<0.05). AS-exosomes cocultured with HC CD4+ T cells induced significant upregulation of IFNα2 and IL-33 (q<0.05). Exosomes from patients with AS inhibited the proliferation of regulatory T cells (Treg), suggesting a mechanism for chronically activated T cells in this disease. Culture of CD4+ T cells from healthy individuals in the presence of AS-exosomes reduced the proliferation of FOXP3+ Treg cells and decreased the frequency of FOXP3+IRF4+ Treg cells. miRNA sequencing identified 24 differentially expressed miRNAs found in circulating exosomes of patients with AS compared with HC; 22 of which were upregulated and 2 were downregulated.ConclusionsIndividuals with AS have different immunological and genetic profiles, as determined by evaluating the exosomes of these patients. The inhibitory effect of exosomes on Treg in AS suggests a mechanism contributing to chronically activated T cells in this disease.

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LncRNA HOTTIP impacts the proliferation and differentiation of fibroblast-like synoviocytes in ankylosing spondylitis through the microRNA-30b-3p/PGK1 axis

Cited by 3 publications

References 44 publications

A review of long non-coding RNAs in ankylosing spondylitis: pathogenesis, clinical assessment, and therapeutic targets

A review of long non-coding RNAs in ankylosing spondylitis: pathogenesis, clinical assessment, and therapeutic targets

Down-regulation of long noncoding RNA HULC inhibits the inflammatory response in ankylosing spondylitis by reducing miR-556-5p-mediated YAP1 expression

Proteomic and genomic profiling of plasma exosomes from patients with ankylosing spondylitis

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