Jizhe Yu1, Yushuang Qin2, Naxin Zhou3. 1. Department of Orthopaedics, Yichang Central People's Hospital, 183 Yiling Avenue, Wujiagang District, Yichang City, 443003, Hubei Province, P. R. China. 2. Department of Nuclear Medicine, Yichang Central People's Hospital, 183 Yiling Avenue, Wujiagang District, Yichang City, 443003, Hubei Province, P. R. China. 3. Department of Orthopaedics, Yichang Central People's Hospital, 183 Yiling Avenue, Wujiagang District, Yichang City, 443003, Hubei Province, P. R. China. znx19681027@sina.cn.
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.
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.
Authors: Carmen C Sucharov; David P Kao; J David Port; Anis Karimpour-Fard; Robert A Quaife; Wayne Minobe; Karin Nunley; Brian D Lowes; Edward M Gilbert; Michael R Bristow Journal: JCI Insight Date: 2017-01-26
Authors: William W Du; Chao Zhang; Weining Yang; Tianqiao Yong; Faryal Mehwish Awan; Burton B Yang Journal: Theranostics Date: 2017-09-26 Impact factor: 11.556