Circ_0045714 alleviates TNF-α-induced chondrocyte injury and extracellular matrix degradation through miR-218-5p/HRAS axis

Jiang, Haitao; Dai, Jiangdong; Zhang, Cheng; Sun, Hailang; Tang, Xiaoming

doi:10.1007/s10863-020-09868-y

Cited by 11 publications

(5 citation statements)

References 28 publications

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“…Here, circ_0045714 expression was found to be lower in both knee cartilage tissues and cells from OA patients than normal controls, which was in favor with previous data [ 14 , 28 ]. Besides, we discovered a down-regulation of circ_0045714 in IL-1β-insulted HAC, and this finding was consistent with the finding in TNF-α-induced OA model in HAC [ 15 , 28 ]. Moreover, we noticed that circ_0045714 was resistant to RNase R digestion and actinomycin D (a transcriptional inhibitor) treatment.…”

Section: Discussionsupporting

confidence: 79%

“…Accidently, Fang et al [ 16 ] also proposed that circ_0045714 up-regulation could be the molecular mechanism of the relief of OA both in vitro and in vivo. Moreover, reinforcing circ_0045714 had been previously demonstrated to alleviate HAC under TNF-α stress via regulating the proliferation, apoptosis, ECM synthesis, and inflammation [ 15 , 28 ]. Classically, we identified a novel ceRNA axis of circ_0045714 via targeting miR-331-3p and modulating PIK3R3.…”

Section: Discussionmentioning

confidence: 99%

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Circ_0045714/miR-331-3p interaction affects IL-1β-evoked human articular chondrocyte injury through regulating PIK3R3 in a ceRNA regulatory cascade

Ding

Zhou

et al. 2021

J Orthop Surg Res

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Background Osteoarthritis (OA) is characterized by joint pain and joint function limitation. Hsa_circ_0045714 (circ_0045714) is a novel OA-related circular RNA. However, its repertoire remains to be further clarified in joint chondrocytes. Methods RNA and protein expression levels and inflammatory factor levels were detected by real-time quantitative polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay. Cell proliferation and apoptosis were determined by colony formation assay, cell counting kit-8 assay and apoptosis assay. Direct interaction was predicted by bioinformatics method and confirmed by dual-luciferase reporter assay. Results Expression of circ_0045714 and phosphoinositide-3-kinase (PI3K) regulatory subunit 3 (PIK3R3) was declined, and microRNA (miR)-331-3p was promoted in knee articular cartilages and cells from OA patients, as well as interleukin (IL)-1β-challenged human articular chondrocytes (HAC) cell line. In stimulation of IL-1β, HAC cells showed a loss of colony formation ability, cell viability and expression of Bcl-2 and Collagen II, allied with an increase in apoptosis rate and levels of IL-6, IL-8 and tumor necrosis factor-α, Bcl-2-associated X protein, cleaved caspase-3, and ADAM with thrombospondin motif-5. Noticeably, overexpressing circ_0045714 and inhibiting miR-331-3p could suppress IL-1β-evoked these effects, and both were through up-regulating PIK3R3, a key gene in PI3K/AKT signaling pathway. Mechanically, circ_0045714 functioned as competing endogenous RNA (ceRNA) for miR-331-3p and further regulated expression of the downstream target gene PIK3R3. Conclusion There was a novel circ_0045714/miR-331-3p/PIK3R3 ceRNA axis in HAC, and its inhibition might be one mechanism of HAC injury in OA.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Circ_0045714/miR-331-3p interaction affects IL-1β-evoked human articular chondrocyte injury through regulating PIK3R3 in a ceRNA regulatory cascade

Ding

Zhou

et al. 2021

J Orthop Surg Res

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“…The miR-7, miR-27a, and miR-218-5p were reported to inhibit the activity of the PI3K/Akt/mTOR signaling pathway, thus enhancing autophagy and inhibiting the apoptosis of chondrocytes. 271 – 273 In addition, exosomes derived from MSCs in the sub-patellar fat pad protected mice from DMM-induced OA partially by promoting autophagy through suppression of mTOR by miR-100-5p. 274 …”

Section: Pathogenic Pathways and Moleculesmentioning

confidence: 99%

Osteoarthritis: pathogenic signaling pathways and therapeutic targets

Yao

Tao

et al. 2023

Sig Transduct Target Ther

294

147

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Osteoarthritis (OA) is a chronic degenerative joint disorder that leads to disability and affects more than 500 million population worldwide. OA was believed to be caused by the wearing and tearing of articular cartilage, but it is now more commonly referred to as a chronic whole-joint disorder that is initiated with biochemical and cellular alterations in the synovial joint tissues, which leads to the histological and structural changes of the joint and ends up with the whole tissue dysfunction. Currently, there is no cure for OA, partly due to a lack of comprehensive understanding of the pathological mechanism of the initiation and progression of the disease. Therefore, a better understanding of pathological signaling pathways and key molecules involved in OA pathogenesis is crucial for therapeutic target design and drug development. In this review, we first summarize the epidemiology of OA, including its prevalence, incidence and burdens, and OA risk factors. We then focus on the roles and regulation of the pathological signaling pathways, such as Wnt/β-catenin, NF-κB, focal adhesion, HIFs, TGFβ/ΒΜP and FGF signaling pathways, and key regulators AMPK, mTOR, and RUNX2 in the onset and development of OA. In addition, the roles of factors associated with OA, including MMPs, ADAMTS/ADAMs, and PRG4, are discussed in detail. Finally, we provide updates on the current clinical therapies and clinical trials of biological treatments and drugs for OA. Research advances in basic knowledge of articular cartilage biology and OA pathogenesis will have a significant impact and translational value in developing OA therapeutic strategies.

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“…The expression of circ 0045714 in knee cartilage tissues and cells of OA patients was lower than that of normal controls, and circ 0045714 could regulate chondrocyte homeostasis by regulating various miRNAs. It is found that the up-regulation of circ 0045714 inhibited TNF-α-induced chondrocyte growth inhibition, inflammation, and ECM degradation by inhibiting the miR-218-5p/HRAS axis ( Jiang et al, 2021a ). While melatonin could inhibit collagenase-induced OA ( Hong et al, 2014 ), it suggested that melatonin may interact with circ 0045714 when regulating TNF-α.…”

Section: The Role Of Ncrnas In Osteoarthritis and Its Interaction Wit...mentioning

confidence: 99%

The therapeutic effect and mechanism of melatonin on osteoarthritis: From the perspective of non-coding RNAs

et al. 2022

Front. Genet.

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Osteoarthritis (OA) is a slowly progressing and irreversible joint disease. The existing non-surgical treatment can only delay its progress, making the early treatment of OA a research hotspot in recent years. Melatonin, a neurohormone mainly secreted by the pineal gland, has a variety of regulatory functions in different organs, and numerous studies have confirmed its therapeutic effect on OA. Non-coding RNAs (ncRNAs) constitute the majority of the human transcribed genome. Various ncRNAs show significant differentially expressed between healthy people and OA patients. ncRNAs play diverse roles in many cellular processes and have been implicated in many pathological conditions, especially OA. Interestingly, the latest research found a close interaction between ncRNAs and melatonin in regulating the pathogenesis of OA. This review discusses the current understanding of the melatonin-mediated modulation of ncRNAs in the early stage of OA. We also delineate the potential link between rhythm genes and ncRNAs in chondrocytes. This review will serve as a solid foundation to formulate ideas for future mechanistic studies on the therapeutic potential of melatonin and ncRNAs in OA and better explore the emerging functions of the ncRNAs.

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Circ_0045714 alleviates TNF-α-induced chondrocyte injury and extracellular matrix degradation through miR-218-5p/HRAS axis

Cited by 11 publications

References 28 publications

Circ_0045714/miR-331-3p interaction affects IL-1β-evoked human articular chondrocyte injury through regulating PIK3R3 in a ceRNA regulatory cascade

Circ_0045714/miR-331-3p interaction affects IL-1β-evoked human articular chondrocyte injury through regulating PIK3R3 in a ceRNA regulatory cascade

Osteoarthritis: pathogenic signaling pathways and therapeutic targets

The therapeutic effect and mechanism of melatonin on osteoarthritis: From the perspective of non-coding RNAs

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