Knockdown of Circ_SLC39A8 protects against the progression of osteoarthritis by regulating miR-591/IRAK3 axis

被引:9
|
作者
Yu, Jizhe [1 ]
Qin, Yushuang [2 ]
Zhou, Naxin [1 ]
机构
[1] Yichang Cent Peoples Hosp, Dept Orthopaed, 183 Yiling Ave, Yichang City 443003, Hubei, Peoples R China
[2] Yichang Cent Peoples Hosp, Dept Nucl Med, 183 Yiling Ave, Yichang City 443003, Hubei, Peoples R China
关键词
Osteoarthritis; Circ_SLC39A8; miR-591; IRAK3;
D O I
10.1186/s13018-021-02323-7
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
BackgroundThe 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.MethodsThe 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.ResultsCirc_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.ConclusionOur 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.
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页数:10
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