Abstract
BackgroundMicroRNAs (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.MethodsExpression 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.ResultsGAS2 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.ConclusionOur data showed that miR-520c-3p might regulate the GAS2 to inhibit the progression of OA.
Highlights
IntroductionMicroRNAs (miRNAs) have been shown to be associated with osteoarthritis (OA) progression
MicroRNAs have been shown to be associated with osteoarthritis (OA) progression
We found that the overexpression of Growth arrest-specific 2 (GAS2) was able to reverse the protective effect of miR520c-3p on Interleukin 1 beta (IL-1β)-induced chondrocyte apoptosis
Summary
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. Osteoarthritis (OA) is degenerative disease and is a major cause of pain and physical disability [1]. 15% of the global population suffer from OA [2]. Genetics, aging, obesity, and mechanical stress are the primary causes of OA [3]. Clinical therapy for OA includes nonsteroidal anti-inflammatory drugs (NSAIDs), platelet-rich plasma (PRP), or hyaluronic acid (HA) injections [4, 5]. There are numerous factors involved in the development of OA, IL-1β has been reported to play a dominant role in the pathogenesis of OA. IL-1β can significantly increase cartilage damage and used to mimic OA in vitro studies [9].
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