ArticleJournal of orthopaedic surgery and research2023
Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis.
Article in Journal of orthopaedic surgery and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Elucidating the Mechanism of Liver and Kidney Damage in Rats Caused by Exposure to 2,4-Dichlorophenoxyacetic Acid and the Protective Effect ofInternational journal of molecular sciences · 2025Article
- Plasma and synovial fluid extracellular vesicles display altered microRNA profiles in horses with naturally occurring post-traumatic osteoarthritis: an exploratory study.Journal of the American Veterinary Medical Association · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOsteoarthritis (OA) is a chronic disease of the bones and joints that commonly affects middle-aged and elderly individuals, characterized by the degeneration of articular cartilage and inflammation of the joints. The molecular mechanisms of OA urgently need to be further examined. Our study intended to uncover circ-NFKB1/miR-203a-5p/ERBB4 axis in regulating interleukin-1β (IL-1β) induced chondrocytes apoptosis.
methodsGSE178724, GSE79258 and GSE169077 were downloaded from Gene Expression Omibus (GEO) database and differentially expressed circRNAs, miRNAs and mRNAs were obtained by R software. Annexin V assay was used to determine cell apoptosis rate. ELISA was further performed to identify the inflammation response. Dual-luciferase reporter gene assay was conducted to examine the combination among circ-NFKB1, miR-203a-5p and ERBB4.
resultsOur research demonstrated that circ-NFKB1 and ERBB4 were significantly upregulated through bioinformatic analysis. MiR-203a-5p was significantly downregulated through bioinformatic analysis. Silencing of circ-NFKB1 notably inhibited the IL-1β induced chondrocytes apoptosis and upregulated ERBB4 expression. Through prediction on bioinformatics analysis, miR-203a-5p was the target binding circ-NFKB1, and ERBB4 was the potential target of miR-203a-5p. Subsequently, these changes induced by the silencing of circ-NFKB1 were reversed upon addition of pcDNA/ERBB4.
conclusionsSilencing circ-NFKB1 could sponge miR-203a-5p to regulate ERBB4 expression and alleviate OA progression.
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Registered trials
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