长链非编码 RNA SNHG9 在骨关节炎中表达下调，并通过甲基化下调 miR-34a 抑制软骨细胞凋亡。
LncRNA SNHG9 is downregulated in osteoarthritis and inhibits chondrocyte apoptosis by downregulating miR-34a through methylation.
机构信息
Department of arthritis, Affiliated Hospital of Weifang Medical University, No.2428, Yuhe Road, Kuiwen District, Weifang City, Shandong Province, 261031, P.R. China.
Weifang Medical University, NO.4948 Shengli East Street, Weifang City, Shandong Province, 261042, P.R. China.
出版信息
BMC Musculoskelet Disord. 2020 Aug 1;21(1):511. doi: 10.1186/s12891-020-03497-7.
BACKGROUND
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 therefore carried out to investigate the potential interaction between SNHG9 and miR-34a in OA.
METHODS
A 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.
RESULTS
We 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.
CONCLUSION
In conclusion, SNHG9 is downregulated in OA and inhibits chondrocyte apoptosis by downregulating miR-34a through methylation.
背景
我们的初步 RNA-Seq 数据显示，小核仁 RNA 宿主基因 9（SNHG9）在骨关节炎（OA）中的表达发生改变，并且与 miR-34a 呈反向相关，miR-34a 可以调节大鼠 OA 模型中的软骨细胞凋亡。因此，本研究旨在研究 SNHG9 和 miR-34a 在 OA 中的潜在相互作用。
方法
本研究共纳入 60 名健康志愿者（对照组）和 60 名 OA 患者（OA 组）。进行转染、RT-qPCR、甲基化特异性 PCR（MSP）和细胞凋亡检测。
结果
我们发现 SNHG9 在 OA 中下调，并且仅在 OA 样本中，其表达与 miR-34a 的表达呈负相关，而在健康对照样本中则无相关性。在 OA 患者的软骨细胞中，SNHG9 的过表达导致 miR-34a 的下调和 miR-34a 基因的甲基化增加。相比之下，在健康对照者的软骨细胞中，SNHG9 的过表达并不影响 miR-34a 的表达和 miR-34a 基因的甲基化。细胞凋亡分析表明，SNHG9 的过表达通过 miR-34a 导致 OA 患者的软骨细胞凋亡率降低，但对健康对照者的软骨细胞没有影响。
结论
总之，SNHG9 在 OA 中下调，通过甲基化下调 miR-34a 抑制软骨细胞凋亡。
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