Abstract
BackgroundOur preliminary RNA-Seq data revealed altered expression of small nucleolar RNA host gene 9 (SNHG9) in osteoarthritis (OA) and its reverse correlation with miR-34a, which can regulate chondrocyte apoptosis in rat OA model. This study was therefore carried out to investigate the potential interaction between SNHG9 and miR-34a in OA.MethodsA total of 60 healthy volunteers (Control group) as well as 60 OA patients (OA group) were enrolled in this study. Transfections, RT-qPCR, methylation-specific PCR (MSP) and cell apoptosis assay were performed.ResultsWe found that SNHG9 was downregulated in OA and its expression was reversely correlated with the expression of miR-34a only across OA samples but not healthy control samples. In chondrocytes from OA patients, overexpression of SNHG9 led to downregulation of miR-34a and increased methylation of miR-34a gene. In contrast, in chondrocytes from healthy controls, overexpression of SNHG9 did not affect the expression of miR-34a and the methylation of miR-34a gene. Cell apoptosis analysis showed that overexpression of SNHG9 led to decreased apoptotic rate of chondrocytes from OA patients but not chondrocytes from the healthy controls through miR-34a.ConclusionIn conclusion, SNHG9 is downregulated in OA and inhibits chondrocyte apoptosis by downregulating miR-34a through methylation.
Highlights
Our preliminary RNA-Seq data revealed altered expression of small nucleolar RNA host gene 9 (SNHG9) in osteoarthritis (OA) and its reverse correlation with miR-34a, which can regulate chondrocyte apoptosis in rat OA model
The expression of SNHG9 and miR-34a was altered in OA Expression levels of SNHG9 and miR-34a in synovial fluid from both OA patients (n = 60) and controls (n = 60) were measured using RT-qPCR to detect their differential expression in OA
Altered expression of SNHG9 and miR-34a may participate in OA
Summary
Our preliminary RNA-Seq data revealed altered expression of small nucleolar RNA host gene 9 (SNHG9) in osteoarthritis (OA) and its reverse correlation with miR-34a, which can regulate chondrocyte apoptosis in rat OA model. This study was carried out to investigate the potential interaction between SNHG9 and miR-34a in OA. Osteoarthritis (OA) as the most commonly diagnosed joint disease is caused by the breakdown of cartilage in a joint as well as underlying bone [1]. Osteoarthritis mainly affects elderly and causes chronic pain, resulting in disability [2]. The development of novel anti-OA therapies is mainly limited by the unclear molecular mechanisms of this disease [5, 6]. Investigations of the molecular players involved in this disease are of great importance
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