MicroRNAs interfere with DNA methylation in rheumatoid arthritis synovial fibroblasts

Gaur, Niharika; Karouzakis, Emmanuel; Glück, Selene; Bagdonas, Edvardas; Jüngel, Astrid; Michel, Beat A.; Frank-Bertoncelj, Mojca; Neidhart, Michel

doi:10.1136/rmdopen-2016-000299

Cited by 19 publications

(15 citation statements)

References 26 publications

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“…In addition to ER stress, betaine also inhibits apoptosis. In a recent study of rheumatoid arthritis synovial fibroblasts, Gaur and colleagues found that transcription factor-3 (ATF-3), an apoptosis-related molecule, is downregulated by betaine ( 131 ). In addition, betaine can inhibit caspase family proteins.…”

Section: Anti-inflammatory Effects Of Betaine On Diseasesmentioning

confidence: 99%

Betaine in Inflammation: Mechanistic Aspects and Applications

et al. 2018

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Betaine is known as trimethylglycine and is widely distributed in animals, plants, and microorganisms. Betaine is known to function physiologically as an important osmoprotectant and methyl group donor. Accumulating evidence has shown that betaine has anti-inflammatory functions in numerous diseases. Mechanistically, betaine ameliorates sulfur amino acid metabolism against oxidative stress, inhibits nuclear factor-κB activity and NLRP3 inflammasome activation, regulates energy metabolism, and mitigates endoplasmic reticulum stress and apoptosis. Consequently, betaine has beneficial actions in several human diseases, such as obesity, diabetes, cancer, and Alzheimer’s disease.

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Section: Anti-inflammatory Effects Of Betaine On Diseasesmentioning

confidence: 99%

Betaine in Inflammation: Mechanistic Aspects and Applications

et al. 2018

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“…MiRNAs post-transcriptionally regulate the degradation and translation of their target genes. MiRNAs are involved in the inflammatory response and the development of autoimmune diseases, such as rheumatoid arthritis [14], and multiple sclerosis [15]. Increasing evidence has shown that aberrant miRNA expression is linked to the regulation of autophagy [16].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-199a-5p Induced Autophagy and Inhibits the Pathogenesis of Ankylosing Spondylitis by Modulating the mTOR Signaling via Directly Targeting Ras Homolog Enriched in Brain (Rheb)

Wang

Luo

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Ankylosing spondylitis (AS) is an inflammatory and immune disease leading to disability. Autophagy has been identified as a potential player in understanding the pathogenesis of AS. Methods: MiRNA-199a-5p and autophagy-related gene expression were determined by qRT-PCR or Western blot. Cytokine production was determined using ELISA assays. Proliferation was determined by MTT assay. MiRNA-199a-5p and Ras homolog enriched in brain (Rheb) were upregulated or downregulated by overexpression of plasmid or siRNA transfection. Results: Expression of miRNA-199a-5p, and autophagy-related genes LC3, beclin1, and ATG5 was significantly decreased in T cells of AS patients. Serum concentrations of TNF-α, IL-17, and IL-23 were promoted in AS patients, compared to healthy controls. MiRNA-199a-5p expression levels also showed significant negative correlations with the Ankylosing Spondylitis Disease Activity Score (ASDAS) and modified Stoke Ankylosing Spon dylitis Spinal Score (mSASSS) of AS patients. In Jurkat T cells and T cells isolated from AS patients, miRNA-199a-5p overexpression promoted autophagy-related genes expression and decreased TNF-α, IL-17, and IL-23 levels, whereas inhibition of miRNA-199a-5p attenuated these effects. As a direct target of miRNA-199a-5p, Rheb inhibition led to a striking decrease in the phosphorylation of the mechanistic target of rapamycin (mTOR) and induced autophagy. Moreover, pcDNA3.1-Rheb effectively reduced the inhibiting effects of mTOR signaling caused by miRNA-199a-5p overexpression. All effects were offset by pretreating with rapamycin (an mTOR antagonist). Conclusions: AS patients with advanced spinal damage had decreased autophagy levels and that miRNA-199a-5p may induce autophagy and inhibit the pathogenesis of AS by modulating the mTOR signaling via direct targeting Rheb.

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“…The DNA methyltransferase (DNMT)3A was defined as a target of miR-29 in RA-FLS. Thus, miR-29 might repress the remethylation effect of bethaine [40]. Miao et al showed that miR-152 was downregulated in an arthritis rat model, and the overexpression of miR-152 in FLS decreased the expression of DNMT1.…”

Section: Dna Methylation-related Micrornas In Ra-flsmentioning

confidence: 99%

Recent findings regarding the effects of microRNAs on fibroblast-like synovial cells in rheumatoid arthritis

Iwamoto

Kawakami

2019

Immunological Medicine

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Rheumatoid arthritis (RA) is a systemic autoimmune disease with severe joint inflammation and destruction characterized by marked hyperplasia of the lining layer of the synovium. Fibroblast-like synovial cells (FLS) is a key cellular component within the synovia; it plays pivotal roles in RA pathogenesis by unfavorable behaviors such as producing inflammatory cytokines and chemokines, and hyperproliferation. MicroRNAs are evolutionarily conserved small non-coding RNAs (length is 18-25 nucleotides) that regulate gene expression at the post-transcriptional level. There is increasing interest in the involvement of microRNAs in autoimmune diseases including RA. Recent studies revealed the regulation of the function of FLS by microRNAs. Here, we review the known functional microRNAs in RA and summarize the potential uses of these small molecules in the treatment of RA.

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MicroRNAs interfere with DNA methylation in rheumatoid arthritis synovial fibroblasts

Cited by 19 publications

References 26 publications

Betaine in Inflammation: Mechanistic Aspects and Applications

Betaine in Inflammation: Mechanistic Aspects and Applications

MicroRNA-199a-5p Induced Autophagy and Inhibits the Pathogenesis of Ankylosing Spondylitis by Modulating the mTOR Signaling via Directly Targeting Ras Homolog Enriched in Brain (Rheb)

Recent findings regarding the effects of microRNAs on fibroblast-like synovial cells in rheumatoid arthritis

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