Circular RNAs (circRNAs) have been shown to be significant regulators in osteoarthritis (OA), whereas the functional effect of circ_0020014 in OA remains unclear. Our goal was to try and understand the underlying regulatory mechanism of circ_0020014 in OA. The cartilage tissue was obtained from OA patients and trauma patients. Interleukin-1β (IL-1β)-treated chondrocytes (CHON-001) were used as the in vitro cellular model for OA. The expression levels of circ_0020014, microRNA-613 (miR-613), and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) were examined by real-time quantitative polymerase chain reaction (RT-qPCR). The protein level was detected using the western blot assay. Cell viability and apoptosis were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and flow cytometry assays, respectively. The secretion of inflammatory cytokine was determined by enzyme-linked immunosorbent assay (ELISA). Circ_0020014 was upregulated in OA cartilage tissues and IL-1β-treated CHON-001 cells, compared with that in healthy cartilage tissues and untreated cells. IL-1β treatment induced cell injury by promoting inflammation and apoptosis, and inhibiting cell viability and extracellular matrix (ECM) accumulation in chondrocytes. Circ_0020014 knockdown significantly protected CHON-001 cells from IL-1β-induced cell dysfunction. MiR-613 was targeted by circ_0020014 and negatively regulated ADAMTS5 expression. In addition, miR-613 downregulation or ADAMTS5 overexpression partly lessened the protective effect of circ_0020014 knockdown on IL-1β-treated CHON-001 cells. Collectively, circ_0020014 acted as a miR-613 sponge to regulate ADAMTS5 expression, thereby protecting chondrocytes from IL-1β-induced inflammatory damage, which might be a novel diagnostic marker for OA.

中文翻译：

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环状 RNA circ_0020014 通过 miR-613/ADAMTS5 轴促进骨关节炎进展。

环状 RNA (circRNA) 已被证明是骨关节炎 (OA) 的重要调节因子，而 circ_0020014 在 OA 中的功能作用仍不清楚。我们的目标是尝试了解 circ_0020014 在 OA 中的潜在调控机制。软骨组织取自OA患者和创伤患者。白细胞介素-1β (IL-1β) 处理的软骨细胞 (CHON-001) 用作 OA 的体外细胞模型。通过实时定量聚合酶链式反应 (RT-qPCR) 检测 circ_0020014、microRNA-613 (miR-613) 以及具有血小板反应蛋白基序 5 的去整合素和金属蛋白酶 (ADAMTS5) 的表达水平。使用蛋白质印迹法检测蛋白质水平。通过 3-(4, 5-dimethylthiazol-2-yl)-2 测量细胞活力和凋亡，分别进行 5-二苯基-2H-四唑-3-溴化铵 (MTT) 和流式细胞术测定。通过酶联免疫吸附试验（ELISA）测定炎性细胞因子的分泌。与健康软骨组织和未处理细胞相比，Circ_0020014 在 OA 软骨组织和经 IL-1β 处理的 CHON-001 细胞中上调。IL-1β 治疗通过促进炎症和细胞凋亡以及抑制细胞活力和细胞外基质 (ECM) 在软骨细胞中的积累来诱导细胞损伤。Circ_0020014 敲低显着保护 CHON-001 细胞免受 IL-1β 诱导的细胞功能障碍。MiR-613 被 circ_0020014 靶向并负调控 ADAMTS5 表达。此外，miR-613 下调或 ADAMTS5 过表达部分降低了 circ_0020014 敲低对 IL-1β 处理的 CHON-001 细胞的保护作用。