Le Peng1, Ming Deng1, Yonggang Ma1, Wei Hu1, Fan Liang2. 1. Department of Orthopaedics, Renmin Hospital of Wuhan University, No. 238, Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, China. 2. Department of Orthopaedics, Renmin Hospital of Wuhan University, No. 238, Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, China. li99770@163.com.
Abstract
BACKGROUND: MicroRNAs (miRNAs) have been shown to be associated with osteoarthritis (OA) progression. This study aimed to explore the role of miR-520c-3p in OA progression. METHODS: Expression levels of miR-520c-3p and Growth arrest-specific 2 (GAS2) were detected using quantitative real-time PCR. The proliferation and apoptosis of cells were measured using cell counting kit 8 (CCK8) assay and flow cytometry. Furthermore, the protein levels of apoptosis-related markers, extracellular degradation markers, inflammatory response markers, and GAS2 were tested using quantitative real-time polymerase chain reaction (RT-PCR) and western blot (WB) analysis. In addition, the interaction between miR-520c-3p and GAS2 was examined using dual luciferase reporter assay. RESULTS: GAS2 was highly expressed, and miR-520c-3p was lowly expressed in OA cartilage tissues. miR-520c-3p could promote the proliferation and inhibit the apoptosis and inflammation of OA chondrocytes. miR-520c-3p could be sponged by GAS2, and its inhibitor could reverse the regulation of GAS2 on the biological functions of OA chondrocytes. GAS2 was a target of miR-520c-3p, which was identified by bioinformatic analysis and dual-luciferase reporter assay. Overexpression of GAS2 could inhibit the proliferation and promoted the apoptosis and inflammation of OA chondrocytes. CONCLUSION: Our data showed that miR-520c-3p might regulate the GAS2 to inhibit the progression of OA.
BACKGROUND: MicroRNAs (miRNAs) have been shown to be associated with osteoarthritis (OA) progression. This study aimed to explore the role of miR-520c-3p in OA progression. METHODS: Expression levels of miR-520c-3p and Growth arrest-specific 2 (GAS2) were detected using quantitative real-time PCR. The proliferation and apoptosis of cells were measured using cell counting kit 8 (CCK8) assay and flow cytometry. Furthermore, the protein levels of apoptosis-related markers, extracellular degradation markers, inflammatory response markers, and GAS2 were tested using quantitative real-time polymerase chain reaction (RT-PCR) and western blot (WB) analysis. In addition, the interaction between miR-520c-3p and GAS2 was examined using dual luciferase reporter assay. RESULTS:GAS2 was highly expressed, and miR-520c-3p was lowly expressed in OA cartilage tissues. miR-520c-3p could promote the proliferation and inhibit the apoptosis and inflammation of OA chondrocytes. miR-520c-3p could be sponged by GAS2, and its inhibitor could reverse the regulation of GAS2 on the biological functions of OA chondrocytes. GAS2 was a target of miR-520c-3p, which was identified by bioinformatic analysis and dual-luciferase reporter assay. Overexpression of GAS2 could inhibit the proliferation and promoted the apoptosis and inflammation of OA chondrocytes. CONCLUSION: Our data showed that miR-520c-3p might regulate the GAS2 to inhibit the progression of OA.
Authors: Enrico Ragni; Alison Coluccio; Eleonora Rolli; José Manuel Rodriguez-Peña; Gaia Colasante; Javier Arroyo; Aaron M Neiman; Laura Popolo Journal: Eukaryot Cell Date: 2006-12-22
Authors: Giuseppe Musumeci; Paola Castrogiovanni; Francesca Maria Trovato; Annelie Martina Weinberg; Mohammad K Al-Wasiyah; Mohammed H Alqahtani; Ali Mobasheri Journal: Int J Mol Sci Date: 2015-08-31 Impact factor: 5.923