miR-10b-5p is a novel Th17 regulator present in Th17 cells from ankylosing spondylitis

Chen, L; Al-Mossawi, Hussein; Ridley, A; Sekine, Takuya; Hammitzsch, Ariane; Wit, Jelle de; Simone, Davide; Shi, Hui; Penkava, Frank; Kurowska‐Stolarska, Mariola; Pulyakhina, Irina; Knight, Julian C.; Kim, Tae‐Jong; Bowness, Paul

doi:10.1136/annrheumdis-2016-210175

Cited by 62 publications

(49 citation statements)

References 16 publications

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“…11 Currently, miRNAs have been speculated as therapeutic targets for improving AS treatment due to its aberrant expression in the T helper 17 cells from AS patients. 22 Meanwhile, the involvement of miRNAs as mediators has been implicated in various biological processes linked to the osteoblasts, such as apoptosis, metabolism, differentiation, proliferation, and bone formation, which provide a theoretical reference for targeting miRNAs in treating metabolic bone diseases. 23 Therefore, our study investigated the role of miR-96 in osteoblast differentiation and bone formation of AS.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐96 promotes osteoblast differentiation and bone formation in ankylosing spondylitis mice through activating the Wnt signaling pathway by binding to SOST

Wang

et al. 2019

J of Cellular Biochemistry

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Ankylosing spondylitis (AS) refers to a type of arthritis manifested with chronic inflammation of spine joints. microRNAs (MiRNAs) have been identified as new therapeutic targets for inflammatory diseases. In this study, we evaluated the influence of microRNA‐96 (miR‐96) on osteoblast differentiation together with bone formation in a murine model of AS. The speculated relationship that miR‐96 could bind to sclerostin (SOST) was verified by dual luciferase reporter assay. After successful model establishment, the mice with AS and osteoblasts isolated from mice with AS were treated with mimics or inhibitors of miR‐96, or DKK‐1 (a Wnt signaling inhibitor). The effects of gain‐ or loss‐of‐function of miR‐96 on the inflammatory cytokine release (IL‐6, IL‐10, and TNF‐α), alkaline phosphatase (ALP) activity, calcium nodule formation, along with the viability of osteoblasts were determined. It was observed that miR‐96 might target and regulate SOST. Besides, miR‐96 was expressed at a high level in AS mice while SOST expressed at a low level. TOP/FOP‐Flash luciferase reporter assay confirmed that miR‐96 activated the Wnt signaling pathway. Moreover, AS mice overexpressing miR‐96 exhibited increased contents of IL‐6, IL‐10 and TNF‐α, ALP activity, calcium nodule numbers, and viability of osteoblasts. In contrast, inhibition of miR‐96 resulted in suppression of the osteoblast differentiation and bone formation. In conclusion, the study implicates that overexpressing miR‐96 could improve osteoblast differentiation and bone formation in AS mice via Wnt signaling pathway activation, highlighting a potential new target for AS treatment.

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Section: Discussionmentioning

confidence: 99%

microRNA‐96 promotes osteoblast differentiation and bone formation in ankylosing spondylitis mice through activating the Wnt signaling pathway by binding to SOST

Wang

et al. 2019

J of Cellular Biochemistry

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“…IL-21 participates in HIV-1 control in vivo via inducing microRNA-29 (miR-29) [30]. And IL-17A would be suppressed by miR-10b to participate the pathological processes of ankylosing spondylitis [31]. Moreover, IL-34 modulates HCC metastasis through microRNA-28 [32].…”

Section: Discussionmentioning

confidence: 99%

Interleukin-34 inhibits hepatitis B virus replication in vitro and in vivo

et al. 2017

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BackgroundThe hepatitis B virus (HBV) infection could activate the immune system and induce extensive inflammatory response. As the most important inflammatory factor, interleukins are critical for anti-viral immunity. Here we investigated whether interleukin-34 (IL-34) play a role in HBV infection.Methodology/Principal findingsIn this study, we first found that both serum IL-34 and IL-34 mRNA in PBMCs in chronic HBV patients was significantly decreased compared to the healthy controls. Furthermore, both IL-34 protein and mRNA levels were declined hepatoma cells expressing HBV. In addition, the clinical parameters analysis found that serum IL-34 was significantly associated with HBV DNA (P = 0.0066), ALT (P = 0.0327), AST (P = 0.0435), TB (P = 0.0406), DB (P = 0.0368) and AFP (P = 0.0225). Correlation analysis also found that serum IL-34 negatively correlated with HBV DNA copies, ALT and AST. In vitro studies found that IL-34 treatment in HepAD38 and HepG2.2.15 cells markedly inhibited HBV DNA, total RNA, 3.5kb mRNA and HBc protein. In vivo studies further demonstrated IL-34 treatment in HBV transgenic mice exhibited greater inhibition on HBV DNA, total RNA, 3.5kb mRNA and HBc protein, suggesting the effect to IL-34 on HBV is likely due to host innate or adaptive immune response.Conclusions/SignificanceOur study identified a novel interleukin, IL-34, which has anti-viral activity in HBV replication in hepatocytes in vitro and in vivo. These data suggest a rationale for the use of IL-34 in the HBV treatment.

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“…Aside from let‐7i and miR‐130a, a recent study reported that AS Th17 cells increased expression of the miR‐10b‐5p, miR‐155‐5p, and miR‐210‐3p. Chen et al () further described the function of one of these, miR‐10b, in the regulation of cytokine production by Th17 cells. IL‐6 and TNF‐α increased expression of the miR‐10b, which in turn inhibited IL‐17A production.…”

Section: Biogenesis Of Mirnasmentioning

confidence: 99%

MicroRNA implications in the etiopathogenesis of ankylosing spondylitis

Mohammadi

Hemmatzadeh

Babaie

et al. 2018

Journal Cellular Physiology

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Ankylosing spondylitis (AS) is a chronic immune-mediated inflammatory disease that affects both axial and peripheral skeletons as well as soft tissues. Recent investigations offer that disease pathogenesis is ascribed to a complex interplay of genetic, environmental, and immunological factors. Until now, there is no appropriate method for early diagnosis of AS and the successful available therapy for AS patients stay largely undefined. MicroRNAs (miRNAs), endogenous small noncoding RNAs controlling the functions of target mRNAs and cellular processes, are present in human plasma in a stable form and have appeared as possible biomarkers for activity, pathogenesis, and prognosis of the disease. In the present review, we have tried to summarize the recent findings related to miRNAs in AS development and discuss the possible utilization of these molecules as prognostic biomarkers or important therapeutic strategies for AS. Further examinations are needed to determine the unique miRNAs signatures in AS and characterize the mechanisms mediated by miRNAs in the pathology of this disease.

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miR-10b-5p is a novel Th17 regulator present in Th17 cells from ankylosing spondylitis

Cited by 62 publications

References 16 publications

microRNA‐96 promotes osteoblast differentiation and bone formation in ankylosing spondylitis mice through activating the Wnt signaling pathway by binding to SOST

microRNA‐96 promotes osteoblast differentiation and bone formation in ankylosing spondylitis mice through activating the Wnt signaling pathway by binding to SOST

Interleukin-34 inhibits hepatitis B virus replication in vitro and in vivo

MicroRNA implications in the etiopathogenesis of ankylosing spondylitis

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