Potential Novel Prediction of TMJ-OA: MiR-140-5p Regulates Inflammation Through Smad/TGF-β Signaling

Li, Weihao; Zhao, Shurong; Yang, Hefeng; Zhang, Chao; Kang, Qiang; Xu, Yeqiong; Ding, Yu; Li, Song

doi:10.3389/fphar.2019.00015

Cited by 31 publications

(23 citation statements)

References 44 publications

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“…To date, multiple targets of miR-140-5p have been identified as cartilage matrix modulators during the progression of OA from inflammation, chondrocyte hypertrophy and senescence to cartilage matrix degradation. miR-140-5p was found to inhibit inflammation by directly targeting Toll-like receptor (TLR)-4, C-X-C motif chemokine receptor (CXCR)-4, mothers against decapentaplegic homologue (SMAD) 3 [42], and interleukin-1 beta (IL-1β) [39]. Additionally, the inhibitory effect of miR-140-5p in chondrocyte hypertrophy has been shown through targeting histone deacetylase (HDAC)-4 [48] and SMAD1 [47].…”

Section: Mir-140 Targetsmentioning

confidence: 99%

Recent progress on the role of miR-140 in cartilage matrix remodelling and its implications for osteoarthritis treatment

Liang

et al. 2020

Arthritis Res Ther

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Cartilage matrix remodelling homeostasis is a crucial factor in maintaining cartilage integrity. Loss of cartilage integrity is a typical characteristic of osteoarthritis (OA). Strategies aimed at maintaining cartilage integrity have attracted considerable attention in the OA research field. Recently, a series of studies have suggested dual functions of microRNA-140 (miR-140) in cartilage matrix remodelling. Here, we discuss the significance of miR-140 in promoting cartilage formation and inhibiting degeneration. Additionally, we focused on the role of miR-140 in the chondrogenesis of mesenchymal stem cells (MSCs). Of note, we carefully reviewed recent advances in MSC exosomes for miRNA delivery in OA treatment.

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Section: Mir-140 Targetsmentioning

confidence: 99%

Recent progress on the role of miR-140 in cartilage matrix remodelling and its implications for osteoarthritis treatment

Liang

et al. 2020

Arthritis Res Ther

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“…Under the condition of diabetes, alterations in internal environmental factors, such as hyperglycaemia, hyperlipidaemia, hypertonic states, and microbial infection, cause changes in genetic information and affect the expression and regular activities of several miRNAs by intron transcription of host genes (Baker et al, 2017 ). The abnormal expression of miRNAs in serum and kidney tissues [such as let-7p, miR-140-5p (Li W. et al, 2019 ), miR-146a, miR-155-3p (Marques-Rocha et al, 2018 ), miR-29c, miR-31, miR-33a, and miR-451 (Graham et al, 2015 )] regulates the mRNA and protein expression of inflammatory cytokines by activating or inhibiting related signal transduction processes, causing the kidney to produce more of cytokines.…”

Section: Micrornas Cytokines and Dnmentioning

confidence: 99%

MicroRNAs as Regulators of Immune and Inflammatory Responses: Potential Therapeutic Targets in Diabetic Nephropathy

Zhou

Meng

et al. 2021

Front. Cell Dev. Biol.

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Diabetic nephropathy (DN) is the principal cause of end-stage renal disease and results in high morbidity and mortality in patients, causing a large socioeconomic burden. Multiple factors, such as metabolic abnormalities, inflammation, immunoregulation and genetic predisposition, contribute to the pathogenesis of DN, but the exact mechanism is unclear, and the therapeutic strategies are not satisfactory. Accordingly, there is an unmet need for new therapeutic targets and strategies for DN. MicroRNAs (miRNAs) act as major epigenetic mechanisms that regulate gene expression and provide novel insights into our understanding of the molecular and signaling pathways that are associated with various diseases, including DN. Studies in the past decade have shown that different miRNAs affect the progression of DN by modulating different aspects of immune and inflammatory responses. Therefore, in this review, we summarized the pivotal roles of miRNAs in inflammatory and immune processes, with an integrative comprehension of the detailed signaling network. Additionally, we discussed the possibilities and significance of these miRNAs as therapeutic targets in the treatment of DN. This review will facilitate the identification of new therapeutic targets and novel strategies that can be translated into clinical applications for DN treatment.

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“…Whether and how the convergence of NF-κB and TGF-β signaling participate in inflammation-mediated hypertrophy of chondrocyte in OA was not clearly understood. Previous reports showed that IL-1β and TNFα could inhibit TGF-β-induced SMAD2/3 transcriptional activity 29 . And down-regulation of IL-1β and TNFα induced by LBP was accompanied by up-regulation of TGFβ1 30 .…”

Section: Discussionmentioning

confidence: 96%

Targeting miR-18a sensitizes chondrocytes to anticytokine therapy to prevent osteoarthritis progression

Lian

Tao

et al. 2020

Cell Death Dis

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Inflammation participates in the development of OA and targeting inflammatory signaling pathways is a potential strategy for OA treatment. IL-1β is one of the most important inflammatory factors to trigger the activation of NF-κB signaling and accelerate OA progression, whereas OA patients could hardly benefit from inhibiting IL-1β in clinic, suggesting the importance to further explore the details of OA inflammation. We here showed that expression of miR-18a in chondrocytes was specifically induced in response to IL-1β in vitro as well as in rat model of OA during which NF-κB signaling was involved, and that nuclear-translocated p65 directly upregulated miR-18a expression at transcriptional level. Further, increased miR-18a mediated hypertrophy of chondrocytes, resulting in OA degeneration, by targeting TGFβ1, SMAD2, and SMAD3 and subsequently leading to repression of TGF-β signaling. And the level of serum miR-18a was positively correlated to severity of OA. Interestingly, other than IL-1β, pro-inflammation cytokines involving TNFα could also remarkably upregulate miR-18a via activating NF-κB signaling and subsequently induce chondrocytes hypertrophy, suggesting a pivotal central role of miR-18a in inflammatory OA progression. Thus, our study revealed a novel convergence of NF-κB and TGF-β signaling mediated by miR-18a, and a novel mechanism underlying inflammation-regulated OA dependent of NF-κB/miR-18a/TGF-β axis. Notably, in vivo assay showed that targeting miR-18a sensitized OA chondrocytes to IL-1β inhibitor as targeting IL-1β and miR-18a simultaneously had much stronger inhibitory effects on OA progression than suppressing IL-1β alone. Therefore, the diagnostic and therapeutic potentials of miR-18a for OA were also revealed.

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Potential Novel Prediction of TMJ-OA: MiR-140-5p Regulates Inflammation Through Smad/TGF-β Signaling

Cited by 31 publications

References 44 publications

Recent progress on the role of miR-140 in cartilage matrix remodelling and its implications for osteoarthritis treatment

Recent progress on the role of miR-140 in cartilage matrix remodelling and its implications for osteoarthritis treatment

MicroRNAs as Regulators of Immune and Inflammatory Responses: Potential Therapeutic Targets in Diabetic Nephropathy

Targeting miR-18a sensitizes chondrocytes to anticytokine therapy to prevent osteoarthritis progression

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