Altered Expression of MicroRNAs in Rheumatoid Arthritis

Tavasolian, Fataneh; Abdollahi, Elham; Rezaei, Ramin; Momtazi‐Borojeni, Amir Abbas; Henrotin, Yves; Sahebkar, Amirhossein

doi:10.1002/jcb.26205

Cited by 72 publications

(56 citation statements)

References 80 publications

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“…2 The management of RA is limited to retarding the progression of the disease, improving functional capacity, and relieving pain. With regard to RA, miRNAs may serve as potential biomarkers for both diagnosis and prognosis for RA, 5 with, in particular, evidence for miR-146a/b upregulation in RA synovial tissue, 6 and miR-125 upregulation in peripheral blood mononuclear cells and plasma posttreatment. 3 miRNAs are a class of endogenous, single-stranded, noncoding RNAs with about 22 nucleotides.…”

Section: Introductionmentioning

confidence: 99%

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Zhong

Yang

et al. 2018

J of Cellular Biochemistry

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Recently, it has been accepted that miR-based therapy may be beneficial for rheumatoid arthritis (RA). This study aimed to evaluate the potential involvement of miR-145 in RA in vitro. The expression of miR-145 in the human fibroblast-like synoviocyte line MH7A was overexpressed by miR-mimic transfection, after which cells were subjected to lipopolysaccharides (LPS). Cell viability, apoptosis, and the release of pro-inflammatory cytokines were measured. The result showed that the apoptosis and the release of IL-1β, IL-6, IL-8, and TNF-α were significantly induced by LPS. Meanwhile, LPS treatment led to downregulation of miR-145. miR-145 overexpression in LPS-untreated MH7A cells had no impacts on cell apoptosis and inflammation. But, restoring miR-145 expression in LPS-stimulated cells by supplementation of a miR-145 mimic protected MH7A cells against LPS-induced apoptosis and inflammation. Furthermore, miR-145 overexpression in LPS-untreated MH7A cells slightly blocked the PI3K/ATK and mTOR pathways, whereas miR-145 overexpression in LPS-stimulated cells notably repressed the LPS-induced activation of PI3K/ATK and MAPK/mTOR pathways. Our study suggested that miR-145 protected MH7A cells against LPS-induced apoptosis and inflammation by inhibiting the PI3K/AKT and MAPK/mTOR pathways.

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Section: Introductionmentioning

confidence: 99%

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Zhong

Yang

et al. 2018

J of Cellular Biochemistry

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“…Accumulating publications have suggested aberrantly expressed or dysfunctional miRNAs may serve as novel biomarkers for rheumatic diseases . During the past few years, circulating miRNAs have drawn much attention in autoimmune diseases including rheumatic diseases .…”

Section: Discussionmentioning

confidence: 99%

MiR‐548a‐3p regulates inflammatory response via TLR4/NF‐κB signaling pathway in rheumatoid arthritis

Wang

Zheng

Gao

et al. 2018

J of Cellular Biochemistry

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Currently published studies have implicated that microRNAs (miRNAs) including exosomes-encapsulated miRNAs play a critical role in rheumatoid arthritis (RA). Previously, we have found that exosomes-encapsulated miR-548a-3p was significantly decreased in serum samples from RA patients by miRNAs microarray analysis. However, little is known of the role of miR-548a-3p in the development and progression of RA. In this study, we aim to investigate the underlying molecular mechanisms of miR-548a-3p in RA, which will provide new insight into understanding the pathogenesis of RA and identifying novel therapeutics targets for this disease. As validated by quantitative real-time polymerase chain reaction (qRT-PCR), the expression of miR-548a-3p in serum exosomes and peripheral blood mononuclear cells (PBMCs) of RA patients (n = 76) was obviously down-regulated compared with healthy controls (n = 20). Serum exosomal miR-548a-3p was negatively associated with levels of CRP, RF, and ESR in serum of patients with RA. MiR-548a-3p could inhibit the proliferation and activation of pTHP-1 cells by regulating the TLR4/NF-κB signaling pathway. Accordingly, exosomes-delivered miR-548a-3p may be a critical factor predicting the disease activity of RA. MiR-548a-3p/TLR4/NF-κB axis can serve as promising targets for RA diagnosis and treatment.

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“…Many miRs have been reported to play a critical role in the regulation of many diseased cells, so they have become potential diagnostic or therapeutic targets for a variety of diseases [19,20]. Accumulated studies have reported during the development of RA the abnormal expression of miRs, including miR-155, miR-146a and miR-125 [21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-27b-3p inhibits apoptosis of chondrocyte in rheumatoid arthritis by targeting HIPK2

Zhou

Chen³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Understanding the mechanism of chondrocytes degeneration could provide a new potential therapeutic idea for rheumatoid arthritis (RA) treatment. MicroRNA-27b-3p (miR-27b-3p) has been shown to regulate a variety of cell behaviors in various cell types. However, the role of miR-27b-3p in RA remains unknown. Materials and methods: Expression of miR-27b-3p and HIPK2 in cartilage tissues and chondrocytes was characterized using qRT-PCR and Western blot. MiR-27b-3p was overexpressed or suppressed in chondrocytes to observe the potential role of miR-27b-3p. Results: We found declined miR-27b-3p and elevated HIPK2 in RA tissues and cells using qRT-PCR. Dual-luciferase reporter assay validated HIPK2 is a direct target of miR-27b-3p, confirmed by Western blot results. Pearson correlation presented that there was a significantly negative correlation between miR-27b-3p and HIPK2 mRNA. Overexpression of miR-27b-3p significantly reduced the expression of pro-apoptotic protein c-caspase3 and increased the expression of anti-apoptotic Bcl-2; however, downregulation of miR-27b-3p has a significant effect of inducing apoptosis. Furthermore, overexpression of miR-27b-3p combined with recombinant HIPK2 protein showed the inhibitory effect of miR-27b-3p was abolished by HIPK2. Conclusion: We found declined miR-27b-3p and elevated HIPK2 in RA tissues and cells. Further in vitro studies demonstrated that miR-27b might inhibit chondrocyte apoptosis and thus attenuate RA development by directly inhibiting HIPK2 expression.

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Altered Expression of MicroRNAs in Rheumatoid Arthritis

Cited by 72 publications

References 80 publications

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

MiR‐548a‐3p regulates inflammatory response via TLR4/NF‐κB signaling pathway in rheumatoid arthritis

MicroRNA-27b-3p inhibits apoptosis of chondrocyte in rheumatoid arthritis by targeting HIPK2

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