YY1 regulation by miR-124-3p promotes Th17 cell pathogenicity through interaction with T-bet in rheumatoid arthritis

Lin, Jinpiao; Tang, Jifeng; Lin, Junyu; He, Yujue; Yu, Ziqing; Jiang, Renquan; Yang, Bin; Ou, Qishui

doi:10.1172/jci.insight.149985

Cited by 25 publications

(15 citation statements)

References 40 publications

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“…Some studies had shown that mir-204-5p was involved in proliferation and production of inflammatory cytokines in RA fibroblast-like synoviocytes ( 74 ). In addition, mir-124-3p was involved in the pathogenicity of Th17 cells in RA ( 75 ). Mir-26b-5p might be a novel biomarker for stratification of RA patients and was worth further clinical validation ( 76 ).…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Tang

Zhang

et al. 2022

Front. Immunol.

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BackgroundSevere coronavirus disease 2019 (COVID -19) has led to a rapid increase in mortality worldwide. Rheumatoid arthritis (RA) was a high-risk factor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, whereas the molecular mechanisms underlying RA and CVOID-19 are not well understood. The objectives of this study were to analyze potential molecular mechanisms and identify potential drugs for the treatment of COVID-19 and RA using bioinformatics and a systems biology approach.MethodsTwo Differentially expressed genes (DEGs) sets extracted from GSE171110 and GSE1775544 datasets were intersected to generate common DEGs, which were used for functional enrichment, pathway analysis, and candidate drugs analysis.ResultsA total of 103 common DEGs were identified in the two datasets between RA and COVID-19. A protein-protein interaction (PPI) was constructed using various combinatorial statistical methods and bioinformatics tools. Subsequently, hub genes and essential modules were identified from the PPI network. In addition, we performed functional analysis and pathway analysis under ontological conditions and found that there was common association between RA and progression of COVID-19 infection. Finally, transcription factor-gene interactions, protein-drug interactions, and DEGs-miRNAs coregulatory networks with common DEGs were also identified in the datasets.ConclusionWe successfully identified the top 10 hub genes that could serve as novel targeted therapy for COVID-19 and screened out some potential drugs useful for COVID-19 patients with RA.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Tang

Zhang

et al. 2022

Front. Immunol.

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“…Therefore, histone modification may also be closely related to YY1. Lin et al demonstrated that the regulation of YY1 by miR-124-3p facilitate Th17 cell pathogenicity by interaction with T-bet in RA [32]. Wang et al demonstrated that lncRNA NEAT1 targets fibroblast-like synoviocytes in RA via the miR-410-3p/ YY1 axis [33].…”

Section: Discussionmentioning

confidence: 99%

SIRT1 is transcriptionally repressed by YY1 and suppresses ferroptosis in rheumatoid arthritis

et al. 2023

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Background Sirtuin 1 (SIRT1) is reported downregulated in rheumatoid arthritis (RA), and the protective effects of SIRT1 on tissue damage and organ failure may be related to cellular ferroptosis. However, the exact mechanism by which SIRT1 regulates RA remains unclear. Methods Quantitative real-time PCR (qPCR) and western blot assays were performed to explore the expressions of SIRT1 and Yin Yang 1 (YY1). CCK-8 assay was used for cytoactive detection. The interaction between SIRT1 and YY1 was validated by dual-luciferase reporter gene assay and chromatin immunoprecipitation (ChIP). DCFH-DA assay and iron assay were applied to detect the reactive oxygen species (ROS) and iron ion levels. Results In the serum of RA patients, SIRT1 was downregulated, but YY1 was upregulated. In LPS-induced synoviocytes, SIRT1 could increase cell viability and decrease ROS and iron levels. Mechanistically, YY1 downregulated the expression of SIRT1 by inhibiting its transcription. YY1 overexpression partly revised the effects of SIRT1 on ferroptosis in synoviocytes. Conclusion SIRT1 is transcriptionally repressed by YY1 and inhibits the ferroptosis of synoviocytes induced by LPS, so as to relieve the pathological process of RA. Therefore, SIRT1 might be a new diagnosis and therapeutic target of RA.

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“…Th1 and Th17 cell subsets contribute to inflammation in RA. Many studies have shown that the inhibition of Th1 and Th17 cell subsets can alleviate RA (77)(78)(79). Th2 cell subsets can inhibit Th1 and Th17 cell differentiation and function by secreting IL-4 as a mechanism to antagonize inflammation (80).…”

Section: The Effect Of Dna Methylation On the Differentiation Of Cd4+...mentioning

confidence: 99%

DNA Methylation of T Lymphocytes as a Therapeutic Target: Implications for Rheumatoid Arthritis Etiology

et al. 2022

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Rheumatoid arthritis (RA) is an autoimmune disease that can cause joint damage and disability. Epigenetic variation, especially DNA methylation, has been shown to be involved in almost all the stages of the pathology of RA, from autoantibody production to various self-effector T cells and the defects of protective T cells that can lead to chronic inflammation and erosion of bones and joints. Given the critical role of T cells in the pathology of RA, the regulatory functions of DNA methylation in T cell biology remain unclear. In this review, we elaborate on the relationship between RA pathogenesis and DNA methylation in the context of different T cell populations. We summarize the relevant methylation events in T cell development, differentiation, and T cell-related genes in disease prediction and drug efficacy. Understanding the epigenetic regulation of T cells has the potential to profoundly translate preclinical results into clinical practice and provide a framework for the development of novel, individualized RA therapeutics.

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YY1 regulation by miR-124-3p promotes Th17 cell pathogenicity through interaction with T-bet in rheumatoid arthritis

Cited by 25 publications

References 40 publications

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

Bioinformatics and System Biology Approach to Identify the Influences of COVID-19 on Rheumatoid Arthritis

SIRT1 is transcriptionally repressed by YY1 and suppresses ferroptosis in rheumatoid arthritis

DNA Methylation of T Lymphocytes as a Therapeutic Target: Implications for Rheumatoid Arthritis Etiology

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