CircRNA_0092516 regulates chondrocyte proliferation and apoptosis in osteoarthritis through the miR-337-3p/PTEN axis

Huang, Zhihui; Ma, Wei; Xiao, Jinhuai; Dai, Xiaoyu; Ling, Wanting

doi:10.1093/jb/mvaa119

Cited by 41 publications

(17 citation statements)

References 39 publications

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Section: Discussionmentioning

confidence: 99%

“…Several studies suggested that circRNAs play an important role in the development of OA [ 4 , 5 ]. Huang et al showed that circRNA_0092516 impairs proliferation and promotes apoptosis in IL-1β-stimulated chondrocytes by regulating the miR-337-3p/PTEN axis [ 4 ]. Zhu et al reported that silencing of circGCN1L1 (hsa_circ_0000448) alleviates the symptoms of OA by regulating miR-330-3p and the TNF-α gene in synoviocytes [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

“…Circular RNAs (circRNAs) comprise a class of non-coding RNAs (ncRNAs) with a closed circular structure that is widely represented in the eukaryotic transcriptome [ 4 ]. Different circRNAs play important functions in a wide variety of cells and contribute to various diseases by regulating gene expression at the post-transcriptional level [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Hsa_circ_0134111 promotes osteoarthritis progression by regulating miR-224-5p/CCL1 interaction

Yong-bao

Zhang

2021

Aging

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Mechanical, metabolic, inflammatory, and immune factors contribute to the development of osteoarthritis (OA), a joint disease characterized by cartilage destruction. The circular RNA (circRNA) hsa_circ_0134111 is upregulated in the cartilage of OA patients; however, its potential role in OA pathogenesis and progression remains unexplored. In this study, the effects of hsa_circ_0134111 knockdown were evaluated in primary human chondrocytes treated with IL-1β to simulate OA, as well as in a rat model of OA. Hsa_circ_0134111 expression was upregulated in IL-1β-stimulated chondrocytes. CCK-8 and flow cytometry assays showed that hsa_circ_0134111 knockdown reversed IL-1β-induced cell decline by inhibiting apoptosis. Following prediction analysis of circRNA and miRNA targets, dual-luciferase reporter and silencing/overexpression assays suggested that a regulatory network composed of hsa_circ_0134111, miR-224-5p, and CCL1 modulates IL-1β-mediated OA-like effects in chondrocytes. Accordingly, CCL1 overexpression abrogated the prosurvival effects of hsa_circ_0134111 knockdown in vitro . Moreover, hsa_circ_0134111 silencing in vivo alleviated cartilage destruction in an OA rat model, decreased IL-6 and TNF-α levels in synovial fluid, and downregulated CCL1 expression in the affected joints. These results suggest that hsa_circ_0134111 contributes to OA development by binding to miR-224-5p, thereby releasing the inhibition that miR-224-5p exerts over CCL1.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hsa_circ_0134111 promotes osteoarthritis progression by regulating miR-224-5p/CCL1 interaction

Yong-bao

Zhang

2021

Aging

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“…Circular RNAs (circRNAs) are a class of noncoding RNAs produced by dorsal splicing of precursor mRNAs and are widely expressed in mammals with highly conserved, stable, and tissue-specific patterns [ 16 ]. Because circRNAs are highly expressed, structurally stable, and possess a large number of miRNA binding sites, they may be a “biological sponge”' for enriching miRNAs [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA mmu_circ_0001598 Contributes to IL-1β-Induced Osteoarthritis Progression by Regulating miR-127-3p

Apizi

Talifujiang

Kasimu

et al. 2021

Journal of Healthcare Engineering

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Osteoarthritis (OA), a chronic disease characterized by articular cartilage degeneration, is a leading cause of disability and pain worldwide. Accumulating evidence indicates that circular RNAs (circRNAs) play a critical role in various diseases, but the function of circRNAs in OA remains largely unknown. In this study, we found that circ_0001598 was significantly upregulated in chondrocytes treated with IL-1β and in cartilage tissue from mice with severed anterior cruciate ligament surgery (ACLT) induced OA models. Interference with circ_0001598 in vitro restored IL-1β-induced chondrocyte proliferation and apoptosis. Silencing circ_0001598 significantly alleviated ACLT-induced OA in mice. Mechanistically, knockdown of circ_0001598 affected chondrocyte proliferation, apoptosis, and matrix degradation by regulating miR-127-3p. Taken together, our results demonstrate the fundamental role of circ_0001598 and provide new ideas for the prevention and treatment of osteoarthritis.

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“…Furthermore, in the ethanol-induced myocardial injury, SIRT1 is able to mediate phosphatase and tensin homolog (PTEN), thus affecting mitochondrial apoptosis [ 9 ]. Chondrocyte proliferation and apoptosis are influenced by the miR-337-3p/PTEN axis with altered status in OA [ 10 ]. PTEN also regulates epidermal growth factor receptor (EGFR) ubiquitination, and inactivation of PTEN specifically increases EGFR activity [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

SIRT1 restoration enhances chondrocyte autophagy in osteoarthritis through PTEN-mediated EGFR ubiquitination

Liu

Miao

et al. 2022

Cell Death Discov.

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The pharmacological interventions aimed at activating pathways inducing chondrocyte autophagy or reversing extracellular matrix degradation may be promising approaches for the management of osteoarthritis (OA). Evidence exists suggesting that sirtuin 1 (SIRT1) is involved in the pathogenesis of OA. The present study aimed to explore the regulatory role and downstream mechanisms of SIRT1 in OA. Bioinformatics predictions identified downstream factors phosphatase and tensin homolog (PTEN) and epidermal growth factor receptor (EGFR) in OA. We validated poorly expressed SIRT1 and EGFR and highly expressed PTEN in cartilage tissues of OA patients. OA was induced in vitro by exposing human primary chondrocytes to IL-1β and in vivo by destabilization of the medial meniscus (DMM) in a mouse model. SIRT1 knockdown was found to augment IL-1β-stimulated inflammation and chondrocyte metabolic imbalance. Knockdown of SIRT1 diminished PTEN acetylation and then enhanced PTEN expression. PTEN inactivation decreased EGFR ubiquitination and promoted EGFR expression by destabilizing the EGFR-Cbl complex, which in turn inhibited extracellular matrix degradation in cartilage tissues and activated chondrocyte autophagy. In the DMM mouse model, knockdown of SIRT1 inhibited chondrocyte autophagy, promoted metabolic imbalance, thus accelerating osteoarthritic process. In conclusion, SIRT1 represses the ubiquitination of EGFR by down-regulating PTEN, inhibits extracellular matrix degradation and activates chondrocyte autophagy, thereby performing an OA-alleviating role.

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CircRNA_0092516 regulates chondrocyte proliferation and apoptosis in osteoarthritis through the miR-337-3p/PTEN axis

Cited by 41 publications

References 39 publications

Hsa_circ_0134111 promotes osteoarthritis progression by regulating miR-224-5p/CCL1 interaction

Hsa_circ_0134111 promotes osteoarthritis progression by regulating miR-224-5p/CCL1 interaction

Circular RNA mmu_circ_0001598 Contributes to IL-1β-Induced Osteoarthritis Progression by Regulating miR-127-3p

SIRT1 restoration enhances chondrocyte autophagy in osteoarthritis through PTEN-mediated EGFR ubiquitination

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