lncRNA MEG8 is downregulated in osteoarthritis and regulates chondrocyte cell proliferation, apoptosis and inflammation

xlomafota13 shared this article with you from Inoreader lncRNA MEG8 is downregulated in osteoarthritis and regulates chondrocyte cell proliferation, apoptosis and inflammation Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1153. doi: 10.3892/etm.2021.10587. Epub 2021 Aug 10. ABSTRACT Long noncoding RNA (lncRNA) maternally expressed 8, small nucleolar RNA host gene (MEG8) has been widely reported for its pro-proliferative, anti-apoptotic and anti-inflammatory effects in diverse diseases. The aim of the present study was to investigate the effects and underlying mechanism of MEG8 on IL-1β-stimulated human osteoarthritis (OA) chondrocytes. C28/I2 chondrocytes were cultured under the stimulation of IL-1β to establish a cellular model of OA. Functional assays involving Cell Counting Kit-8 and flow cytometry were performed to determine proliferation and apoptosis in the cells. The protein expression levels of caspase-3 and inflammatory cytokines were detected using cell-based ELISA. The expression levels of PI3K/AKT pathway-related proteins were evaluated by western blotting. It was identified that MEG8 expression was increased i n the cartilage of patients with OA and in IL-1β-treated C28/I2 cells. In C28/I2 cells, silencing of MEG8 expression noticeably triggered IL-1β-induced proliferation suppression, cell death and an inflammatory response. However, transfection with MEG8 displayed adverse effects. Furthermore, MEG8 overexpression prevented IL-1β-induced activation of the PI3K/AKT signaling pathway in C28/I2 cells. These data demonstrated that MEG8 exerted protective effects against IL-1β-induced apoptosis and inflammation of OA chondrocytes by regulating the PI3K/AKT signaling pathway. Thus, the present study demonstrates that MEG8 might be a promising target for the treatment of OA. PMID:34504598 | PMC:PMC8393379 | DOI:10.3892/etm.2021.10587 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.