miR-218-5p靶向HMGB1参与脂多糖诱导的足细胞损伤

被引：3

作者：

于群 ^{[1
]}

马启启 ^{[2
]}

王倩惠 ^{[2
]}

林建功 ^{[1
]}

李燕梅 ^{[1
]}

郭齐 ^{[1
]}

机构：

[1] 山东大学附属省立医院肾内科

[2] 山东第一医科大学附属省立医院肾内科

来源：

免疫学杂志 | 2022年 / 38卷 / 02期

关键词：

脂多糖; 足细胞; 高迁移率蛋白B1; miR-218-5p;

D O I：

10.13431/j.cnki.immunol.j.20220016

中图分类号：

R692 [肾疾病];

学科分类号：

摘要：

目的探究miR-218-5p、高迁移率蛋白B1(HMGB1)在脂多糖(LPS)诱导的小鼠足细胞损伤中的作用。方法将小鼠足细胞分为4组:正常对照组、LPS诱导组、HMGB1 shRNA+LPS组、miR-218-5p mimics+LPS组。Western blot和Real-time PCR分别检测各组HMGB1、TLR4、MyD88、TNF-α、IL-6、synaptopodin、ZO-1蛋白和mRNA表达水平;免疫荧光检测synaptopodin、ZO-1的表达和定位;Transwell检测足细胞迁移能力;双荧光素酶报告基因验证miR-218-5p和HMGB1的关系。结果 LPS刺激后,HMGB1、TLR4、MyD88表达明显升高,炎性因子TNF-α、IL-6表达升高,而足细胞标记蛋白synaptopodin、ZO-1表达降低,同时足细胞迁移能力明显增强。沉默HMGB1或过表达miR-218-5p可降低TLR4、MyD88,TNF-α、IL-6表达,增加synaptopodin、ZO-1表达,抑制足细胞迁移能力,缓解足细胞损伤。荧光素酶报告基因检测提示miR-218-5p可直接作用于HMGB1的3’UTR区,调控HMGB1的翻译过程。结论 HMGB1在LPS诱导的足细胞损伤中发挥重要作用,沉默HMGB1或过表达miR-218-5p可通过抑制HMGB1通路,减轻LPS诱导的足细胞炎症反应,缓解足细胞损伤。

引用

页码：108 / 115

页数：8

共 18 条

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