ArticleCartilage2021
LncRNA MEG3 Inhibits the Degradation of the Extracellular Matrix of Chondrocytes in Osteoarthritis via Targeting miR-93/TGFBR2 Axis.
Article in Cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Metamorphosis and lncRNAs: A Close Relationship.Genesis (New York, N.Y. : 2000) · 2026Review
- Review
- IMMT downregulation promotes osteoarthritis development by inducing mitochondrial dysfunction.Journal of orthopaedic surgery and research · 2026Article
- Characterizing the Long Non-Coding RNA Profile of Endometrial Mesenchymal Stem/Stromal Cell-Derived Extracellular Vesicles and Their Anti-Inflammatory Role in Osteoarthritis.International journal of molecular sciences · 2025Article
- Role of long non-coding RNAs in cartilage development and osteoarthritis pathogenesis.European journal of medical research · 2025Review
- Roles of lncRNA in the crosstalk between osteogenesis and angiogenesis in the bone microenvironment.Journal of Zhejiang University. Science. B · 2025Review
- Mechanistic insights into non-coding RNAs regulate autophagy in chondrocytes and their contribution to osteoarthritis.Frontiers in medicine · 2025Review
- CRNDE alleviates IL-1β-induced chondrocyte damage by modulating miR-31/NF-κB pathway.Journal of orthopaedic surgery and research · 2024Article
- Mechanisms of ammonotelism, epithelium damage, cellular apoptosis, and proliferation in gill of Litopenaeus vannamei under NHEnvironmental science and pollution research international · 2024Article
- LncRNA MEG3 suppresses erastin-induced ferroptosis of chondrocytes via regulating miR-885-5p/SLC7A11 axis.Molecular biology reports · 2024Article
- Down-regulation of long noncoding RNA HOXA11-AS nullifies the impact of microRNA-506-3p on chondrocytes proliferation and apoptosis in osteoarthritis.Clinics (Sao Paulo, Brazil) · 2024Article
- Deciphering the Role of LncRNAs in Osteoarthritis: Inflammatory Pathways Unveiled.Journal of inflammation research · 2024Review
- Advances in Research on the Regulatory Roles of lncRNAs in Osteoarthritic Cartilage.Biomolecules · 2023Review
- The emerging role of lncRNAs in osteoarthritis development and potential therapy.Frontiers in genetics · 2023Review
- LncRNA MINCR attenuates osteoarthritis progression via sponging miR-146a-5p to promote BMPR2 expression.Cell cycle (Georgetown, Tex.) · 2022Article
- Knockdown of lncRNA JPX suppresses IL-1β-stimulated injury in chondrocytes through modulating an miR-25-3p/PPID axis.Oncology letters · 2022Article
- LncRNA LEMD1-AS1 relieves chondrocyte inflammation by targeting miR-944/PGAP1 in osteoarthritis.Cell cycle (Georgetown, Tex.) · 2022Article
- The Role of Mitochondrial Metabolism, AMPK-SIRT Mediated Pathway, LncRNA and MicroRNA in Osteoarthritis.Biomedicines · 2022Review
- Downregulation of the LncRNA MEG3 Promotes Osteogenic Differentiation of BMSCs and Bone Repairing by Activating Wnt/β-Catenin Signaling Pathway.Journal of clinical medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a degenerative joint disease, osteoarthritis (OA) is characterized by articular cartilage degradation. Long noncoding RNAs (lncRNAs) act critical roles in the regulation of OA development, including affecting the proliferation, apoptosis, extracellular matrix (ECM) degradation, and inflammatory response of chondrocytes. The current study's aim was to investigate the regulatory function and the underlying molecular mechanism of lncRNA MEG3 in ECM degradation of chondrocytes in OA.
methodsIn the current study, chondrocytes were induced by interleukin-1β (IL-1β) to simulate OA condition, and further assessed cell viability, lncRNA MEG3 and miR-93 expression levels. Overexpression or knockdown of lncRNA MEG3 in chondrocytes treated with IL-1β were performed to investigate the function of MEG3 in regulating cell proliferation, apoptosis and ECM degradation using EdU assay, flow cytometry, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blot. The interaction between MEG3 and miR-93 was assessed using qRT-PCR. Furthermore, overexpression of miR-93 was performed as recovery experiment to explore the functional mechanism of MEG3.
resultsMEG3 was significantly downregulated in chondrocytes treated with IL-1β, whereas miR-93 was upregulated concomitantly. Overexpression of MEG3 induced the proliferation, suppressed the apoptosis, and relieved the degradation of ECM in IL-1β-induced chondrocytes. By contrast, knockdown of MEG3 suppressed the proliferation, promoted the apoptosis, and aggravated ECM degradation in IL-1β induced chondrocytes. In addition, MEG3 was found to relieve the inhibitive expression of TGFBR2 as a competitive endogenous RNA (ceRNA) of miR-93, and then activated transforming growth factor-β (TGF-β) signaling pathway, regulated chondrocytes ECM degradation in IL-1β induced chondrocytes subsequently.
conclusionLncRNA MEG3 targeted miR-93/TGFBR2 axis, regulated the proliferation, apoptosis and ECM degradation of chondrocytes in OA.
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