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首页> 外文期刊>Journal of King Saud University >High expression of LncRNA-MALAT1 in renal tubular cells induced by high glucose and its promotion role on pyroptosis by regulating miR-206
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High expression of LncRNA-MALAT1 in renal tubular cells induced by high glucose and its promotion role on pyroptosis by regulating miR-206

机译：LNCRNA-MALAT1在高葡萄糖诱导的肾小管细胞中的高表达及其通过调节MIR-206对糊衰的促进作用

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BackgroundDiabetic nephropathy (DN) is the main reason for renal failure in terminal stage. Studies have shown that long-chain non-coding RNA (LncRNA) improves DN by regulating microRNA (miR). The study intended to investigate the role of MALAT1/miR-206 on high glucose (HG)-induced inflammation, oxidative stress and cell death of renal tubular epithelial cells (RTECs).MethodsHG-intervened HK-2 cells to establish DN cell model. Transfection effect was confirmed by qRT-PCR and MALAT1, NLRP3, Caspase-1, IL-1β, GSMDD-N and miR-206 were tested. Western blot was performed to test the proteins in NLRP3, Caspase-1, IL-1β and GSMDD-N, and to observe the pyroptosis. Elisa kit was applied to detect TNF-α, IL-6 and MCP-1.ResultsDouble luciferase report experiment and RNA immunoprecipitation (RIP) confirmed that MALAT1 could bind to miR-206. HG induced MALAT1 in HK-2 cells increased. Knocking down MALAT1 could reduce TNF-α, IL-6 and MCP-1. In HG-intervened HK-2 cells, the over-expressed miR-206 transfected into the cells was consistent with the changes of inflammatory factors and cytokines after knock-down MALAT1.ConclusionUp-regulation MALAT1 could reverse the inhibition of miR-206 on pyroptosis and inflammatory response. MALAT1 can improve HG-induced HK-2 pyroptosis by targeting miR-206, which is expected to be a latent target to treat DN in clinic.
机译：背景糖尿病肾病（DN）是终端肾功能衰竭的主要原因。研究表明，通过调节MicroRNA（MIR）来改善DN的长链非编码RNA（LNCRNA）。该研究旨在探讨Malat1 / miR-206对高葡萄糖（Hg）诱导的炎症，氧化应激和细胞死亡的作用，肾小管上皮细胞（Retecs）.methodshg-snovered HK-2细胞建立DN细胞模型。通过QRT-PCR和MALAT1，NLRP3，Caspase-1，IL-1β，GSMDD-N和MIR-206确认转染效应。进行蛋白质印迹以测试NLRP3，Caspase-1，IL-1β和GSMDD-N中的蛋白质，并观察糊酶。 ELISA试剂盒用于检测TNF-α，IL-6和MCP-1.Resultsdouble Luciferase报告实验和RNA免疫沉淀（RIP）证实Malat1可以与miR-206结合。 HG诱导HK-2细胞MALAT1增加。击倒马拉特1可以减少TNF-α，IL-6和MCP-1。在HG介入的HK-2细胞中，转染到细胞中的过度表达的miR-206与爆震后的炎症因子和细胞因子的变化一致。结论 - 调节Malat1可以逆转MiR-206对糊衰的抑制作用和炎症反应。马拉特1可以通过靶向miR-206来改善Hg诱导的HK-2糊凋亡，预计将成为治疗诊所DN的潜在靶标。

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