Diabetic nephropathy (DN) is a common chronic complication of diabetes. In this study, we aimed to explore the potential role of lncRNA LINC-00162 in the pathogenic process of DN. LncRNA microarray analysis, real-time PCR, IHC computational analysis and luciferase assay were performed to explore the regulatory relationship among LINC00162, miR-383 and HDAC9. There was an obvious difference between T2D + DN and T2D - DN patients in their levels of eGRF and albuminuria. A significant difference was observed between T2D + DN and T2D - DN groups in terms of their LINC00162 expression. In particular, LINC00162 and HDAC9 were highly expressed, while miR-383 was lowly expressed in tissues derived from the T2D + DN group compared with those in tissues derived from the T2D - DN group. MiR-383 was able to bind to LINC00162, while HDAC9 was a direct downstream target of miR-383 with a complementary miR-383 binding site located in the 3' UTR of HDAC9. LINC00162 reduced miR-383 expression and further up-regulated HDAC9 expression, while miR-383 mimics reduced HDAC9 expression under a dose-dependent manner. In summary, we suggested for the first time that down-regulation of LINC00162 was associated with the development of DN in T2D via the up-regulation of miR-383 expression and reduction of HDAC9 expression.

中文翻译：

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LINC00162通过调节miR-383 / HDAC9信号通路参与糖尿病性肾病的发病机制。

糖尿病肾病（DN）是糖尿病的常见慢性并发症。在这项研究中，我们旨在探讨lncRNA LINC-00162在DN的致病过程中的潜在作用。进行了LncRNA微阵列分析，实时PCR，IHC计算分析和荧光素酶测定，以探讨LINC00162，miR-383和HDAC9之间的调节关系。T2D + DN和T2D-DN患者的eGRF和蛋白尿水平存在明显差异。就其LINC00162表达而言，在T2D + DN和T2D-DN组之间观察到了显着差异。特别地，与源自T2D-DN组的组织相比，LINC00162和HDAC9高表达，而miR-383在源自T2D + DN组的组织中低表达。MiR-383能够结合LINC00162，而HDAC9是miR-383的直接下游靶标，其互补的miR-383结合位点位于HDAC9的3'UTR中。LINC00162降低了miR-383的表达，并进一步上调了HDAC9的表达，而miR-383模仿物以剂量依赖的方式降低了HDAC9的表达。总之，我们首次建议LINC00162的下调与miR-383表达的上调和HDAC9表达的下调在T2D中DN的发生有关。