miR-520c-3p regulates IL-1β-stimulated human chondrocyte apoptosis and cartilage degradation by targeting GAS2

Peng, Lei; Deng, Ming; Ma, Yonggang; Hu, Wei; Fan, Lei

doi:10.1186/s13018-021-02466-7

Cited by 3 publications

(2 citation statements)

References 21 publications

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“…Chondrocytes synthesize extracellular matrix to maintain the structural and functional integrity of the cartilage [ 10 ]. However, chondrocytes are difficult to maintain cartilage homeostasis in response to OA stimulation [ 11 ]. Chondrocytes convert to catabolic cells that secrete matrix-degrading enzymes, such as matrix metalloproteinases (MMPs), and cartilage degeneration was induced when catabolic-degrading effects overwhelm the anabolic-protective function in OA chondrocytes [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-18a-3p improves cartilage matrix remodeling and inhibits inflammation in osteoarthritis by suppressing PDP1

Feng

2022

J Physiol Sci

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Osteoarthritis (OA) is a degenerative disease characterized by synovial inflammation. MiR-18a-3p was reported to be downregulated in knee anterior cruciate ligament of OA patients. In the present study, the specific functions and mechanism of miR-18a-3p in OA were explored. An in vitro model of OA was established using 10 ng/ml IL-1β to treat ATDC5 cells, and medial meniscus instability surgery was performed on Wistar rats to establish in vivo rat model of OA. RT-qPCR revealed that miR-18a-3p was downregulated in IL-1β-stimulated ATDC5 cells. MiR-18a-3p overexpression inhibited secretion of inflammatory cytokines and concentration of matrix metalloproteinases, as shown by ELISA and western blotting. The binding relation between miR-18a-3p and pyruvate dehydrogenase phosphatase catalytic subunit 1 (PDP1) was detected by luciferase reporter assays. MiR-18a-3p targeted PDP1 and negatively regulated PDP1 expression. Results of rescue assays revealed that PDP1 upregulation reserved the suppressive effect of miR-18a-3p overexpression on levels of inflammatory cytokines and matrix metalloproteinases in IL-1β-stimulated ATDC5 cells. H&E staining was used to observe pathological changes of synovial tissues in the knee joint of Wistar rats. Safranin O-fast green/hematoxylin was used to stain cartilage samples of knee joints. MiR-18a-3p overexpression suppressed OA progression in vivo. Overall, miR-18a-3p improves cartilage matrix remodeling and suppresses inflammation in OA by targeting PDP1.

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Section: Introductionmentioning

confidence: 99%

MiR-18a-3p improves cartilage matrix remodeling and inhibits inflammation in osteoarthritis by suppressing PDP1

Feng

2022

J Physiol Sci

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“…Firstly, we found the target gene of lncRNA HAGLR and proved the relationship between miR-130a-3p and lncRNA HAGLR. Existing evidence indicates that IL-1β is increased in arthritic joints, which can cause chondrocyte apoptosis and inflammation [29,30]. In this investigation, CHON-001 cells were exposed to 10 ng/ml IL-1β for 12 h to generate the OA model in vitro.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HAGLR silencing inhibits IL-1β-induced chondrocytes inflammatory injury via miR-130a-3p/JAK1 axis

et al. 2023

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Background Osteoarthritis (OA), the most common form of arthritis, is accompanied by destruction of articular cartilage, development of osteophyte and sclerosis of subchondral bone. This study aims to explore whether lncRNA HAGLR can play a role in OA, and further clarify the potential mechanism. Material and methods StarBase and luciferase reporter assay were applied for predicting and confirming the interaction between lncRNA HAGLR, miR-130a-3p and JAK1. The levels of lncRNA HAGLR and miR-130a-3p were analyzed using quantitative reverse transcription PCR (qRT-PCR). The proliferation, cytotoxicity and apoptosis of CHON-001 cells were evaluated by MTT, lactate dehydrogenase assay (LDH) and Flow cytometry (FCM) analysis, respectively. Moreover, expression of cleaved Caspase3 protein were determined by Western blot assay. The release of inflammatory factors (TNF-α, IL-8, and IL-6) was detected by ELISA. Results lncRNA HAGLR directly targets miR-130a-3p. Level of lncRNA HAGLR was substantially higher and miR-130a-3p level was memorably lower in IL-1β stimulated CHON-001 cells than that in Control group. Furthermore, lncRNA HAGLR silencing alleviated IL-1β induce chondrocyte inflammatory injury, as evidenced by increased cell viability, reduced LDH release, decreased apoptotic cells, inhibited cleaved-Caspase3 expression, and reduced secretion of secretion of inflammatory factors. However, miR-130a-3p-inhibitor reversed these findings. We also found miR-130a-3p directly targeted JAK1 and negatively regulated JAK1 expression in CHON-001 cells. In addition, JAK1-plasmid reversed the effects of miR-130a-3p mimic on IL-1β-induced chondrocytes inflammatory injury. Conclusion Silencing of lncRNA HAGLR alleviated IL-1β-stimulated CHON-001 cells injury through miR-130a-3p/JAK1 axis, revealing lncRNA HAGLR may be a valuable therapeutic target for OA therapy.

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Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis

Kong

Sun

Zhang

et al. 2021

Front. Cell Dev. Biol.

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Osteoarthritis (OA) is a joint disease that is pervasive in life, and the incidence and mortality of OA are increasing, causing many adverse effects on people’s life. Therefore, it is very vital to identify new biomarkers and therapeutic targets in the clinical diagnosis and treatment of OA. ncRNA is a nonprotein-coding RNA that does not translate into proteins but participates in protein translation. At the RNA level, it can perform biological functions. Many studies have found that miRNA, lncRNA, and circRNA are closely related to the course of OA and play important regulatory roles in transcription, post-transcription, and post-translation, which can be used as biological targets for the prevention, diagnosis, and treatment of OA. In this review, we summarized and described the various roles of different types of miRNA, lncRNA, and circRNA in OA, the roles of different lncRNA/circRNA-miRNA-mRNA axis in OA, and the possible prospects of these ncRNAs in clinical application.

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miR-520c-3p regulates IL-1β-stimulated human chondrocyte apoptosis and cartilage degradation by targeting GAS2

Cited by 3 publications

References 21 publications

MiR-18a-3p improves cartilage matrix remodeling and inhibits inflammation in osteoarthritis by suppressing PDP1

MiR-18a-3p improves cartilage matrix remodeling and inhibits inflammation in osteoarthritis by suppressing PDP1

LncRNA HAGLR silencing inhibits IL-1β-induced chondrocytes inflammatory injury via miR-130a-3p/JAK1 axis

Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis

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