Long non-coding RNAs (lncRNAs) are confirmed to be involved in modulating diabetic nephropathy (DN). This study is aimed to explore the regulatory mechanism of lncRNA small nucleolar RNA host gene 15 (SNHG15) on pediatric DN. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG) to produce an in vitro model. The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.

中文翻译：

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SNHG15 敲低通过体外调节 miR-141/ICAM-1 轴抑制儿科患者的糖尿病肾病进展。

长链非编码 RNA (lncRNA) 被证实参与调节糖尿病肾病 (DN)。本研究旨在探讨lncRNA小核仁RNA宿主基因15（SNHG15）对小儿DN的调控机制。人肾小球系膜细胞 (HGMC) 暴露于高葡萄糖 (HG) 以产生体外模型。结果表明，SNHG15 在小儿 DN 组织和 HG 诱导的 HGMC 中显着上调。功能实验表明，SNHG15 的沉默和 miR-141 的过表达都提高了细胞活力，并抑制了 HG 诱导的 HGMC 的炎症。SNHG15被鉴定为可以与miR-141结合的lncRNA，ICAM-1是miR-141的下游靶基因。miR-141的低表达和ICAM-1的高表达均逆转了SNHG15敲低对炎症反应的抑制作用和对细胞活力的促进作用。总之，我们的研究表明，SNHG15 的沉默通过在体外调节 miR-141/ICAM-1 轴来改善小儿 DN 的恶性行为。