The Impact of MicroRNA-223-3p on IL-17 Receptor D Expression in Synovial Cells

Moriya, Nozomu; Shibasaki, Seiji; Karasaki, Miki; Iwasaki, Tsuyoshi

doi:10.1371/journal.pone.0169702

Cited by 23 publications

(14 citation statements)

References 49 publications

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“…Of course, in addition to affecting the TLR4/TLR2/NF-κB/STAT3 signaling pathway and directly affecting the levels of inflammatory factors, miR-223-3p may also impact the expression of inflammatory factors via other pathways, such as miR-223, which is highly expressed in the bone marrow cells and reportedly inhibits IL-6 by targeting the inflammatory body sensor NLRP3 [31]. Further, miR-223-3p may up-regulate the expression of IL-6 in synoviocytes by down-regulating the expression of IL-17 receptor D [32]. In addition, miR-223 affects IL-6 secretion in mast cells via the insulin-like growth factor 1 receptor/PI3K signaling pathway [22].…”

Section: Discussionmentioning

confidence: 99%

Impact of miR-223-3p and miR-2909 on inflammatory factors IL-6, IL-1ß, and TNF-α, and the TLR4/TLR2/NF-κB/STAT3 signaling pathway induced by lipopolysaccharide in human adipose stem cells

Niu

Zhao

et al. 2019

PLoS ONE

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MicroRNAs (miRNAs) are small non-coding RNA molecules that play an important role in the regulation of gene expression related to inflammatory responses. Human adipose stem cells are characterized by pluripotent differentiation potential and isolated from adipose tissues. These cells regulate inflammation mainly by interacting with immune cells and affecting the secretion of immune factors; details of this interaction are currently unknown. In the current study, we successfully established an acute inflammation model and a chronic inflammation model involving adipose stem cells. We used high-throughput miRNA microarray analysis to identify miRNAs that were significantly (p < 0.05) differentially expressed during both acute and chronic inflammation. Lipopolysaccharide (LPS) significantly (p < 0.05) reduced the expression of miR-223-3P and miR-2909, while promoting the production of pro-inflammatory cytokines, interleukin (IL) 6, IL-1β, and tumor necrosis factor (TNF)-α via the Toll-like receptor (TLR) 4/TLR2/nuclear factor (NF)-κB/signal transducer and activator of transcription (STAT) 3 signaling pathway in human adipose stem cells. Further, miR-223-3P expression was significantly (p < 0.05) reduced in human adipose stem cells during activation by IL-6 stimulation. The inducible down-regulation of miR-223-3P resulted in the activation of STAT3, which was directly targeted by miR-223-3P. STAT3 directly targeted TLR4 and TLR2, promoting the production of the pro-inflammatory cytokine, IL-6, and formed a positive feedback loop to regulate IL-6 levels. Similarly, TNF-α significantly (p < 0.05) increased the expression of miR-223-3p, with LPS and TLR4/TLR2/NF-κB/STAT3 forming a negative feedback loop to regulate TNF-α levels. In addition, miR-2909, which depends on NF-κB, targeted Krueppel-like factor (KLF) 4 to regulate the levels of pro-inflammatory cytokines, IL-6, IL-1β, and TNF-α. We conclude that miR-223-3p and miR-2909 form a complex regulatory network with pro-inflammatory factors and signaling pathways in adipose stem cells stimulated by LPS. These findings will inform the development of therapies against autoimmune and inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Impact of miR-223-3p and miR-2909 on inflammatory factors IL-6, IL-1ß, and TNF-α, and the TLR4/TLR2/NF-κB/STAT3 signaling pathway induced by lipopolysaccharide in human adipose stem cells

Niu

Zhao

et al. 2019

PLoS ONE

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“…IL-17RD was found to negatively regulate Toll-like receptor (TLR)-induced immune responses by targeting TIR adaptor protein, which sequentially inhibited the downstream signaling of TLR [ 44 ]. Furthermore, the heteromer of IL-17RD and TNF receptor 2 (TNFR2) has been reported to play a role in the activation of NF-κB signaling [ 45 ], and a relationship between IL-17RD and miR-223-3p has been identified in previous studies [ 46 ]. In the current study, gga-miR122-5p, gga-miR-193b-3p, gga-miR-34b-5p, and miR-223-3p were negatively correlated with IL-17RD during NDV infection, indicating that IL-17RD may play an important role in NDV infection.…”

Section: Discussionmentioning

confidence: 99%

Common microRNA–mRNA Interactions in Different Newcastle Disease Virus-Infected Chicken Embryonic Visceral Tissues

Jia

Wang

et al. 2018

IJMS

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To investigate the roles and explore the altered expression of microRNAs (miRNAs) and mRNAs in chicken embryos in response to Newcastle disease virus (NDV) infection, deep sequencing was performed. Then, a conjoint analysis of small RNA-seq and mRNA-seq was performed to screen interactional miRNA–mRNA pairs during NDV infection. In total, 15 and 17 up- and downregulated miRNAs were identified that potentially targeted 4279 and 6080 mRNAs in NDV-infected chicken embryonic tissues, respectively; in addition, 595 upregulated and 480 downregulated mRNAs were identified. The conjoint analysis of the obtained data identified 1069 miRNA–mRNA pairs. Among these pairs, 130 pairs were related to immune or inflammatory responses. The relationship between gga-miR-203a and its target transglutaminase 2 (TGM2) was confirmed using a dual-luciferase reporter system and a real time quantitative polymerase chain reaction (RT-qPCR) assay. Overall, the discovery of miRNAs, mRNAs, and their potential pairing relationships, which may be involved in the regulation of NDV infection, will facilitate our understanding of the complex regulatory relationship between the host and the virus.

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“…This result was also confirmed by Wu's 2019 study. In addition, miR-223 could also inhibit the expression of inflammatory factors such as IL-6 by targeting NLRP3 [53], upregulate the expression of IL-6 in synoviocytes by downregulating the expression of IL-17 receptor D [54], and, through the IGF-1/PI3K signaling pathway, affect the secretion of IL-6 in mast cells [55]. hypothesize that aerobic exercise could increase the expression of miR-223 in the hippocampus of CUMS-depressed mice and slow down the hippocampal inflammatory response in depressed mice, which is mediated by the activation of the TLR4/MyD88-NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

Aerobic Exercise Inhibits CUMS-Depressed Mice Hippocampal Inflammatory Response via Activating Hippocampal miR-223/TLR4/MyD88-NF-κB Pathway

Hong-lin

Liu

Chen

et al. 2020

IJERPH

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Objective: To investigate the role of aerobic exercise in inhibiting chronic unpredictable mild stress (CUMS) depressed mice hippocampal inflammatory response and its potential mechanisms. Methods: Fifty-four male eight-week-old C57BL/6 mice were divided as control group (CG) (18 mice) and model group (36 mice). Model group mice were treated with 13 chronic stimulating factors for 28 days to set up the CUMS depression model. Neurobehavioral assessment was performed after modeling. The mice in the model group were randomly divided into the control model group (MG) and the aerobic exercise group (EG), with 18mice in each group. The EG group carried out the adaptive training of the running platform: 10 m/min, 0° slope, and increased by 10 minutes per day for 6 days. The formal training was carried for 8 weeks with 10 m/min speed, 0° slope, 60 min/d, 6 d/Week. After the training, a neurobehavioral assessment was performed, and hippocampus IL-1β and IL-10 protein levels were detected by ELISA. RT–PCR was used to detect the expression of miR-223 and TLR4, MyD88, and NF-κB in the hippocampus. Western blot was used to detect the expression of TLR4 and phosphorylated NF-κBp65 protein in the hippocampus. Results: The hippocampus function of CUMS depression model mice was impaired. The forced swimming and forced tail suspension time were significantly prolonged, and inflammatory factors IL-1β were significantly increased in the hippocampus. Aerobic exercise significantly improves CUMS-depressed mice hippocampal function, effectively reducing depressive behavior and IL-1β levels, and increasing IL-10 levels. Besides, aerobic exercise significantly upregulates the expression level of miR-223 and inhibits the high expression of TLR4, MyD88, and NF-κB. Conclusion: Aerobic exercise significantly increases the CUMS-depressed mice hippocampus expression of miR-223, and inhibits the downstream TLR4/MyD88-NF-κB signaling pathway and the hippocampal inflammatory response, which contributes to the improvement of the hippocampal function.

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The Impact of MicroRNA-223-3p on IL-17 Receptor D Expression in Synovial Cells

Cited by 23 publications

References 49 publications

Impact of miR-223-3p and miR-2909 on inflammatory factors IL-6, IL-1ß, and TNF-α, and the TLR4/TLR2/NF-κB/STAT3 signaling pathway induced by lipopolysaccharide in human adipose stem cells

Impact of miR-223-3p and miR-2909 on inflammatory factors IL-6, IL-1ß, and TNF-α, and the TLR4/TLR2/NF-κB/STAT3 signaling pathway induced by lipopolysaccharide in human adipose stem cells

Common microRNA–mRNA Interactions in Different Newcastle Disease Virus-Infected Chicken Embryonic Visceral Tissues

Aerobic Exercise Inhibits CUMS-Depressed Mice Hippocampal Inflammatory Response via Activating Hippocampal miR-223/TLR4/MyD88-NF-κB Pathway

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