ArticleInternational journal of molecular medicine2020
Circular RNA derived from TIMP2 functions as a competitive endogenous RNA and regulates intervertebral disc degeneration by targeting miR‑185‑5p and matrix metalloproteinase 2.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- The circTIMP2/miR-106a/TIMP2 tumor-suppressive axis versus tumor-derived exosomal counteraction in gastric cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- The Prognostic Significance of LINC00638 in Lumbar Disc Herniation and Its Effect on Senescence of Nucleus Pulposus Cells.JOR spine · 2025Article
- Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.International journal of molecular sciences · 2024Review
- The pathological mechanisms of circRNAs in mediating intervertebral disc degeneration.Non-coding RNA research · 2023Review
- tsRNA-04002 alleviates intervertebral disk degeneration by targeting PRKCA to inhibit apoptosis of nucleus pulposus cells.Journal of orthopaedic surgery and research · 2023Article
- Circular RNA and intervertebral disc degeneration: unravelling mechanisms and implications.Frontiers in molecular biosciences · 2023Review
- Identification of novel gene signatures and immune cell infiltration in intervertebral disc degeneration using bioinformatics analysis.Frontiers in molecular biosciences · 2023Article
- Expression and Biological Functions of miRNAs in Chronic Pain: A Review on Human Studies.International journal of molecular sciences · 2022Review
- SNHG5/miR-299-5p/ATF2 Axis as a Biomarker in Immune Microenvironment of Intervertebral Disc Degeneration.Mediators of inflammation · 2022Article
- The Roles of circRNAs in Intervertebral Disc Degeneration: Inflammation, Extracellular Matrix Metabolism, and Apoptosis.Analytical cellular pathology (Amsterdam) · 2022Review
- Exosomes Mediate APP DysregulationFrontiers in cell and developmental biology · 2022Article
- miR-328-5p Induces Human Intervertebral Disc Degeneration by Targeting WWP2.Oxidative medicine and cellular longevity · 2022Article
- Roles of circular RNAs in the pathogenesis of intervertebral disc degeneration (Review).Experimental and therapeutic medicine · 2021Review
- Article
- Genetic Variants and Protein Alterations of Selenium- and T-2 Toxin-Responsive Genes Are Associated With Chondrocytic Damage in Endemic Osteoarthropathy.Frontiers in genetics · 2021Article
- Circular RNAs in Intervertebral Disc Degeneration: An Updated Review.Frontiers in molecular biosciences · 2021Review
- Construction of a Potentially Functional circRNA-miRNA-mRNA Network in Intervertebral Disc Degeneration by Bioinformatics Analysis.BioMed research international · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is an important cause of lower back pain, although the underlying mechanisms remain poorly understood. The present study aimed to examine the role of a circular RNA derived from tissue inhibitor of metallopeptidases 2 (circ‑TIMP2) in degenerative nucleus pulposus (NP) tissues, and to validate its function in cultured human NP cells. Overexpression of miR‑185‑5p in NP cells markedly inhibited the enhanced extracellular matrix (ECM) catabolism induced by tumor necrosis factor‑α (TNF‑α) and interleukin‑1β (IL‑1β) treatment. Bioinformatics analysis demonstrated that matrix metalloproteinase 2 (MMP2) was a potential target of miR‑185‑5p. MMP2 protein expression levels were increased following treatment with TNF‑α and IL‑1β in NP cells compared with those in untreated cells, and this effect was attenuated by transfection with miR‑185‑5p. Compared with normal NP tissues, IDD samples exhibited higher circ‑TIMP2 expression levels. In addition, overexpression of circ‑TIMP2 promoted ECM catabolism and suppressed ECM anabolism. Furthermore, circ‑TIMP2 sequestered miR‑185‑5p, which may potentially upregulate the target genes associated with ECM degradation. In conclusion, the results of the present study revealed that circ‑TIMP2 promoted TNF‑α‑ and IL‑1β‑induced NP cell imbalance between ECM anabolism and catabolism via miR‑185‑5p‑MMP2 signaling. These findings provide a potential therapeutic option for the treatment of IDD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.