CircADAMTS6/miR‐431‐5p axis regulate interleukin‐1β induced chondrocyte apoptosis
Background Growing evidence suggests that circular RNAs (circRNAs) are involved in the development of osteoarthritis (OA). The present study aimed to explore the CircADAMTS6/miR‐431‐5p axis with respect to regulating interleukin‐1β (IL‐1β) induced chondrocyte apoptosis. Methods We first evaluated th...
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Veröffentlicht in: | The journal of gene medicine 2021-02, Vol.23 (2), p.e3304-n/a |
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Sprache: | eng |
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Zusammenfassung: | Background
Growing evidence suggests that circular RNAs (circRNAs) are involved in the development of osteoarthritis (OA). The present study aimed to explore the CircADAMTS6/miR‐431‐5p axis with respect to regulating interleukin‐1β (IL‐1β) induced chondrocyte apoptosis.
Methods
We first evaluated the differentially expressed circRNAs between normal chondrocytes and interleukin (IL)‐1β‐stimulated chondrocytes. Then, bioinformatic analysis was performed to identify the role and function of circADAMTS6. Small interfering RNA‐expressing or overexpressing circADAMTS6 lentiviral vectors were used for transduction of chondrocytes. Annexin‐V‐fluorescein isothiocyanate (FITC) double staining was performed to measure the apoptotic rate of the chondrocytes in each group. Finally, a dual luciferase reporter assay was performed to identify the target relationship between circADAMTS6 and miR‐431‐5p.
Results
After treatment with IL‐1β, circADAMTS6 was down‐regulated compared to the normal chondrocyte group. The overexpression of circADAMTS6 inhibited apoptosis in human chondrocytes, as indicated by annexin‐V‐FITC double staining. However, overexpression of miR‐431‐5p had the opposite effect. A dual luciferase reporter assay indicated that circADAMTS6 could directly binding with miR‐431‐5p.
Conclusions
Our findings demonstrate that the circADAMTS6/miR‐431‐5p axis comprises a new target for OA. Bioinformatic analysis suggested that circADAMTS6 acted as a sponge of miR‐431‐5p.
CircADAMTS6/miR‐431‐5p axis regulate interleukin‐1β induced chondrocyte apoptosis. |
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ISSN: | 1099-498X 1521-2254 |
DOI: | 10.1002/jgm.3304 |