长链非编码 RNA SOX2OT 通过 miR-9/SIRT1 轴诱导自噬减轻高糖诱导的足细胞损伤。
LncRNA SOX2OT alleviates the high glucose-induced podocytes injury through autophagy induction by the miR-9/SIRT1 axis.
机构信息
Departments of Nephrology, The First Affiliated Hospital of Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui 233000, PR China.
Departments of Nephrology, The First Affiliated Hospital of Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui 233000, PR China.
出版信息
Exp Mol Pathol. 2019 Oct;110:104283. doi: 10.1016/j.yexmp.2019.104283. Epub 2019 Jul 10.
OBJECTIVES
Podocytes injury is a major contributor to the progression of diabetic nephropathy (DN). This study aims to investigate the role of long non-coding RNA SOX2OT in the high glucose (HG)-induced injury of human podocytes cells (HPCs) and the underlying mechanism.
METHODS
HPCs proliferation and apoptosis were examined using MTT assay and flow cytometry assay, respectively. The protein levels of SIRT1 and autophagy-associated proteins (Beclin-1, LC3-II, Atg7, and p62) were determined using western blot. The interactions among SOX2OT, miR-9, and SIRT1 were investigated using luciferase activity assay.
RESULTS
SOX2OT overexpression significantly alleviated the HG-induced HPCs injury and induced autophagy, which was abrogated by the autophagy inhibitor 3-MA and SIRT1 knockdown. Mechanistically, SOX2OT acted as a ceRNA by sponging miR-9 to facilitate SIRT1, and thus induce autophagy.
CONCLUSION
SOX2OT overexpression alleviates the HG-induced podocytes injury through autophagy induction by the miR-9/SIRT1 axis.
目的
足细胞损伤是糖尿病肾病（DN）进展的主要原因。本研究旨在探讨长链非编码 RNA SOX2OT 在高糖（HG）诱导的人足细胞（HPC）损伤中的作用及其潜在机制。
方法
分别采用 MTT 法和流式细胞术检测 HPC 增殖和凋亡。Western blot 法检测 SIRT1 及自噬相关蛋白（Beclin-1、LC3-II、Atg7 和 p62）的蛋白水平。采用荧光素酶活性测定法研究 SOX2OT、miR-9 和 SIRT1 之间的相互作用。
结果
SOX2OT 过表达显著减轻 HG 诱导的 HPC 损伤并诱导自噬，自噬抑制剂 3-MA 和 SIRT1 敲低可阻断这种作用。机制上，SOX2OT 通过海绵吸附 miR-9 作为 ceRNA 来促进 SIRT1，从而诱导自噬。
结论
SOX2OT 过表达通过 miR-9/SIRT1 轴诱导自噬减轻 HG 诱导的足细胞损伤。
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