ArticleJournal of bone and mineral metabolism2022
CircTMOD3 promotes lipopolysaccharide-induced chondrocyte apoptosis in osteoarthritis by sponging miR-27a.
Article in Journal of bone and mineral metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Circular RNAs orchestrate molecular networks in osteoarthritis: From miRNA sponging to epigenetic and exosome-mediated regulation.Molecular biology reports · 2026Review
- Recent advancements of miRNAs in the treatment of bone diseases and their delivery potential.Current research in pharmacology and drug discovery · 2023Review
- CircRNAs in osteoarthritis: research status and prospect.Frontiers in genetics · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe progression of osteoarthritis (OA) requires the involvement of lipopolysaccharide (LPS)-induced inflammation, in which circTMOD3 plays an important role. We predicted that circTMOD3 could interact with miR-27a to inhibit LPS-induced chondrocyte apoptosis and explored the interaction between circTMOD3 and miR-27a in OA. MATERIALS AND
methodsTotal RNAs were isolated from cartilage tissue samples from both OA patients (n = 62) and controls (n = 62) and subjected to RT-qPCRs to determine circTMOD3 and miR-27a (mature and premature) expression. Subcellular location of circTMOD3 and its interaction with premature miR-27a were analyzed using subcellular fractionation assay and RNA-RNA pulldown assay, respectively. CircTMOD3 was overexpressed in chondrocytes to study its role in miR-27a maturation. The roles of circTMOD3 and miR-27a in LPS-induced chondrocyte apoptosis were analyzed using cell apoptosis assay.
resultsCircTMOD3 and premature miR-27a levels were increased while mature miR-27a level was decreased in OA. CircTMOD3 was located in both nuclear and cytoplasm fractions of chondrocytes. CircTMOD3 directly interacted with premature miR-27a and promoted LPS-induced chondrocyte apoptosis, while miR-27a inhibited LPS-induced chondrocyte apoptosis. Moreover, circTMOD3 overexpression suppressed miR-27a maturation and reduced the inhibitory effects of miR-27a on LPS-induced chondrocyte apoptosis.
conclusionCircTMOD3 suppresses miR-27a maturation in OA to promote chondrocyte apoptosis induced by LPS.
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