LncRNA NEAT1 regulates chondrocyte proliferation and apoptosis via targeting miR-543/PLA2G4A axis
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RESEARCH ARTICLE
LncRNA NEAT1 regulates chondrocyte proliferation and apoptosis via targeting miR‑543/PLA2G4A axis Peng Xiao1 · Xu Zhu1 · Jinpeng Sun1 · Yuhang Zhang1 · Weijian Qiu1 · Jianqiang Li1 · Xuejian Wu1 Received: 3 June 2020 / Accepted: 11 September 2020 © Japan Human Cell Society 2020
Abstract Osteoarthritis (OA), which is characterized by articular cartilage degeneration, shows a gradually increasing incidence with age. This study explored the molecular mechanism underlying the proliferation and apoptosis of chondrocytes during OA progression. In this study, chondrocytes were isolated from human knee cartilages. The targeted relationship among nuclear enriched abundant transcript 1 (NEAT1), microRNA-543 (miR-543) and PLA2G4A was predicted on TargetScan V7.2 and starBase and validated by performing dual-luciferase reporter assay. High-expressed NEAT1 was detected in OA cartilage and chondrocytes. NEAT1 was negatively correlated with miR-543 and was low-expressed in OA cartilage and PLA2G4A was negatively correlated with miR-543 and was high-expressed in OA cartilage. In OA chondrocytes, the overexpressed NEAT1 inhibited the expressions of p-Akt1 and Bcl-2 and upregulated that of matrix metalloprotease (MMP)-3, MMP-9, MMP-13, interleukin (IL)-6 and IL-8, but such effects of overexpressed NEAT1 were reversed by miR-543 mimic. SiRNANEAT1 exerted an opposite effect to NEAT1 overexpression on OA chondrocytes, but this could be reversed by miR-543 inhibitor. The effect of PLA2G4A overexpression was the opposite to miR-543 mimic on OA chondrocytes. In conclusion, NEAT1 could sponge miR-543 to induce PLA2G4A expression, inhibit chondrocyte proliferation and promote apoptosis. Keywords NEAT1 · miR-543 · PLA2G4A · Chondrocytes · Osteoarthritis
Introduction Osteoarthritis (OA), recognized as the most prevalent chronic joint disease, is characterized by a series of mechanical abnormalities, such as subchondral bone hyperplasia, synovial inflammation and articular cartilage degradation [1–3]. Articular cartilage, a nearly frictionless surface, can endure pressure of several times the body weight [4]. This incredible capability is ascribed to the existence of cartilage extracellular matrix (ECM) that has mechanical properties due to its unique structure and composition [4]. Chondrocytes, surrounded by a narrow matrix region, are located within ECM [4]. The massive releases of inflammatory cytokines initially caused abnormalities of synovium and alteration in cartilage microenvironment, leading to chondrocyte dysfunction [5, 6]. Previous study proposed that * Xuejian Wu [email protected] 1
Department of Orthopedics, The First Affiliated Hospital of Zhengzhou University, No.1, East Jianshe Road, Zhengzhou 450000, Henan Province, China
cartilage degeneration caused by chondrocyte apoptosis and malfunction of articular cartilage rehabilitation triggered by abnormal chondrocyte migration and proliferation are closely associated with the pathogenesis of OA [7, 8]. Therefore, our study sought to discover the regula
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