ArticleClinical rheumatology2020
LncRNA CTBP1-AS2 is upregulated in osteoarthritis and increases the methylation of miR-130a gene to inhibit chondrocyte proliferation.
Article in Clinical rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Single‑cell sequencing, genetics, and epigenetics reveal mesenchymal stem cell senescence in osteoarthritis (Review).International journal of molecular medicine · 2024Review
- Osteoarthritis related epigenetic variations in miRNA expression and DNA methylation.BMC medical genomics · 2023Article
- The emerging role of lncRNAs in osteoarthritis development and potential therapy.Frontiers in genetics · 2023Review
- Long noncoding RNAs in mesenchymal stromal/stem cells osteogenic differentiation: Implications in osteoarthritis pathogenesis.World journal of stem cells · 2022Article
- Long non‑coding RNA CTBP1‑AS2 upregulates USP22 to promote pancreatic carcinoma progression by sponging miR‑141‑3p.Molecular medicine reports · 2022Article
- Epigenetic regulation by long noncoding RNAs in osteo-/adipogenic differentiation of mesenchymal stromal cells and degenerative bone diseases.World journal of stem cells · 2022Review
- Emerging role of lncRNAs in osteoarthritis: An updated review.Frontiers in immunology · 2022Review
- Knockdown of LINC01385 inhibits osteoarthritis progression by modulating the microRNA-140-3p/TLR4 axis.Experimental and therapeutic medicine · 2021Article
- The non-coding RNA interactome in joint health and disease.Nature reviews. Rheumatology · 2021Review
- Knockdown of long non-coding RNA KCNQ1OT1 suppresses the progression of osteoarthritis by mediating the miR-211-5p/TCF4 axisExperimental and therapeutic medicine · 2021Article
- DNA Methylation Signatures of Bone Metabolism in Osteoporosis and Osteoarthritis Aging-Related Diseases: An Updated Review.International journal of molecular sciences · 2021Review
- Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- The Emerging Role of Non-Coding RNAs in Osteoarthritis.Frontiers in immunology · 2021Review
- Interactions Among lncRNA/circRNA, miRNA, and mRNA in Musculoskeletal Degenerative Diseases.Frontiers in cell and developmental biology · 2021Review
- Enrichment of genomic pathways based on differential DNA methylation profiles associated with knee osteoarthritis pain.Neurobiology of pain (Cambridge, Mass.)Article
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4 authors.
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Abstract
objectivesLncRNA CTBP1-AS2 has been reported to be involved in type 2 diabetes and cardiomyocyte hypertrophy, while its roles in other human diseases are unknown. Our preliminary deep sequencing analysis showed altered expression of CTBP1-AS2 in osteoarthritis (OA). In addition, CTBP1-AS2 was inversely correlated with miR-130a. This study was therefore carried out to investigate the interactions between CTBP1-AS2 and miR-130a in OA.
methodsSynovial fluid was collected from 62 OA patients and 62 healthy controls. RT-qPCR was performed to determine the expression levels of CTBP1-AS2 and miR-130a in synovial fluid. Cell transfections were performed to investigate the interactions between CTBP1-AS2 and miR-130a. Methylation-specific PCR (MSP) was performed to assess the effects of CTBP1-AS2 on the methylation of miR-130a. Cell counting Kit-8 (CCK-8) assay was performed to evaluate the roles of CTBP1-AS2 and miR-130a in regulating proliferation of chondrocytes.
resultsThe results showed that CTBP1-AS2 was upregulated in OA and inversely correlated with miR-130a. In chondrocytes of OA patients, overexpression of CTBP1-AS2 led to increased methylation of miR-130a gene and downregulated expression of miR-130a, while overexpression of miR-130a did not affect the expression of CTBP1-AS2. In contrast, no interaction between CTBP1-AS2 and miR-130a was observed in chondrocytes from healthy adults. Analysis of chondrocyte proliferation showed that overexpression of miR-130a led to increased proliferation rate of chondrocytes extracted from OA patients. Overexpression of CTBP1-AS2 led to decreased proliferation rate of chondrocytes and reversed the effects of overexpressing miR-130a.
conclusionTherefore, CTBP1-AS2 is upregulated in OA and may increase the methylation of miR-130a gene to inhibit chondrocyte proliferation. Key Points • CTBP1-AS2 is overexpressed in OA and may downregulate miR-130a through methylation to suppress the proliferation of chondrocytes. • The interaction between CTBP1-AS2 and miR-130a is indirect and mediated by certain pathological mediators.
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