1. Knockdown of Circ_SLC39A8 protects against the progression of osteoarthritis by regulating miR-591/IRAK3 axis.
- Author
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Yu J, Qin Y, and Zhou N
- Subjects
- Aged, Apoptosis genetics, Cell Survival genetics, Cells, Cultured, Chondrocytes physiology, Disease Progression, Down-Regulation genetics, Female, Humans, Interleukin-1 Receptor-Associated Kinases genetics, Male, MicroRNAs genetics, Middle Aged, Osteoarthritis metabolism, Cation Transport Proteins genetics, Cation Transport Proteins physiology, Chondrocytes metabolism, Gene Knockdown Techniques, Interleukin-1 Receptor-Associated Kinases metabolism, MicroRNAs metabolism, Osteoarthritis genetics
- Abstract
Background: The dysregulation of circular RNAs (circRNAs) has been identified in various human diseases, including osteoarthritis (OA). The purpose of this study was to identify the role and mechanism of circ_SLC39A8 in regulating the progression of OA., Methods: The expression levels of circ_SLC39A8, miR-591, and its potential target gene, interleukin-1-receptor-associated kinase 3 (IRAK3), were identified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The relationship between miR-591 and circ_SLC39A8 or IRAK3 was predicted by bioinformatics tools and verified by dual-luciferase reporter., Results: Circ_SLC39A8 and IRAK3 were upregulated and miR-591 was downregulated in OA cartilage tissues. Knockdown of circ_SLC39A8 inhibited apoptosis and inflammation in OA chondrocytes, while these effects were reversed by downregulating miR-591. Promotion cell viability effects of miR-591 were partially reversed by IRAK3 overexpression., Conclusion: Our findings indicated that knockdown of circ_SLC39A8 delayed the progression of OA via modulating the miR-591-IRAK3 axis, providing new insight into the molecular mechanisms of OA pathogenesis.
- Published
- 2021
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