Abstract
BackgroundOsteoarthritis (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.MethodsThe 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.ResultsIn 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.ConclusionSNHG7 sponged miR-34a-5p to affect cell proliferation, apoptosis and autophagy through targeting SYVN1 which provides a novel sight into the pathogenesis of OA.
Highlights
Osteoarthritis (OA) is one of the most common rheumatic diseases of which clinical symptoms includes swelling, synovitis and inflammatory pain, affect patients’ daily life
SNHG7 was down‐regulated in OA tissues To investigate the role of SNHG7 in OA, Quantitative real-time PCR (qRT-PCR) was used to detect the expression of SNHG7 in OA tissues obtained from 15 OA patients and normal tissues obtained from 10 trauma patients
We detected the SNHG7 expression in normal chondrocytes and normal chondrocytes treated with IL-1β and found that SNHG7 was downregulated in IL-1β-treated normal chondrocytes, but the percentage of downregulation was much smaller than that in IL-1β-treated OA cells (Additional file 1: Figure S1)
Summary
Osteoarthritis (OA) is one of the most common rheumatic diseases of which clinical symptoms includes swelling, synovitis and inflammatory pain, affect patients’ daily life. The regulation mechanism of ncRNA in OA pathogenesis has not been fully elucidated. Non-coding RNA (ncRNA) is composed of long noncoding RNA and small non-coding RNA. Studies have reported that ncRNAs have significant regulatory effects on human diseases [9]. Functional studies of lncRNA have shown that it can play an important role in cell development, differentiation and disease occurrence, including OA [12,13,14]. Studies have reported that lncRNAs may acts as competitive RNA which competitively binds to target miRNAs to indirectly regulate mRNAs [15, 16]. LncRNA SNHG7 (small nucleolar RNA host gene 7) has been demonstrated to participate in cell development and progression of many diseases, especially in cancers [17,18,19]. SNHG7 expression was downregulated in OA [21], and the function and regulatory of SNHG7 in OA has not been fully explored
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