Osteoarthritis (OA) is one of the most common rheumatic diseases of which clinical symptoms includes swelling, synovitis and inflammatory pain, affect patients’ daily life. It was reported that non-coding RNAs play vital roles in OA. However, the regulation mechanism of ncRNA in OA pathogenesis has not been fully elucidated. The expression of SNHG7, miR-34a-5p and SYVN1 was detected using qRT-PCR in tissues, serum and cells. The protein expression of SYVN1, PCNA, cleavage-caspase 3, beclin1 and LC3 were measured using western blot. The RNA immunoprecipitation (RIP), RNA pulldown, and luciferase reporter assays were used to verify the relationship between SNHG7, miR-34a-5p and SYVN1. The MTT and flow cytometry assay was performed to detected cell proliferation and cell apoptosis respectively. In this study, SNHG7 and SYVN1 expression were down-regulated, but miR-34a-5p was up-regulated in OA tissues and IL-1β treated cells compared with normal tissues and chondrocyte. Functional investigation revealed that up-regulated SNHG7 or down-regulated miR-34a-5p could promote cell proliferation and inhibit cell apoptosis and autophagy in OA cells. More than that, RIP, pulldown and luciferase reporter assay was applied to determine that miR-34a-5p was a target miRNA of SNHG7 and SYVN1 was a target mRNA of miR-34-5p. Rescue experiments showed that overexpression of miR-34a reversed high expression of SNHG7-mediated suppression of apoptosis and autophagy as well as promotion of proliferation, while its knockdown inhibited cell apoptosis and autophagy and promoted cell proliferation which could be impaired by silencing SYVN1. In addition, SNHG7 regulated SYVN1 through sponging miR-34a-5p. SNHG7 sponged miR-34a-5p to affect cell proliferation, apoptosis and autophagy through targeting SYVN1 which provides a novel sight into the pathogenesis of OA.

中文翻译：

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LncRNA SNHG7 / miR-34a-5p / SYVN1轴在骨关节炎的增殖，凋亡和自噬中起重要作用

骨关节炎（OA）是最常见的风湿性疾病之一，其临床症状包括肿胀，滑膜炎和炎性疼痛，会影响患者的日常生活。据报道，非编码RNA在OA中起着至关重要的作用。但是，尚未完全阐明ncRNA在OA发病机理中的调控机制。使用qRT-PCR检测SNHG7，miR-34a-5p和SYVN1在组织，血清和细胞中的表达。使用蛋白质印迹法检测SYVN1，PCNA，裂解半胱天冬酶3，beclin1和LC3的蛋白表达。RNA免疫沉淀（RIP），RNA下拉和荧光素酶报告基因检测用于验证SNHG7，miR-34a-5p和SYVN1之间的关系。进行MTT和流式细胞仪检测分别检测细胞增殖和细胞凋亡。在这个研究中，与正常组织和软骨细胞相比，在OA组织和经IL-1β处理的细胞中，SNHG7和SYVN1表达下调，但miR-34a-5p上调。功能研究表明，上调的SNHG7或下调的miR-34a-5p可以促进OA细胞的增殖并抑制细胞凋亡和自噬。不仅如此，还应用了RIP，下拉和荧光素酶报告基因检测来确定miR-34a-5p是SNHG7的目标miRNA，而SYVN1是miR-34-5p的目标mRNA。救援实验表明，miR-34a的过表达逆转了SNHG7介导的凋亡和自噬抑制以及增殖促进的高表达，而其敲低则抑制了细胞凋亡和自噬并促进了细胞增殖，而沉默SYVN1可能会削弱它们。此外，SNHG7通过海绵miR-34a-5p调控SYVN1。SNHG7通过靶向SYVN1使miR-34a-5p发挥作用，从而影响细胞增殖，凋亡和自噬，这为OA的发病机理提供了新的视角。