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长链非编码RNA UBE2R2-AS1在糖尿病诱导的肾损伤中的重要作用。

Important role of long non-coding RNA UBE2R2-AS1 in diabetes-induced renal injury.

作者信息

Chen Chuanqi, Yan Yanqiong, Luo Qianjun, Li Sufen

机构信息

Endocrinology Department, Shekou People's Hospital, Nanshan District, Shenzhen, Guangdong, China.

出版信息

Arch Med Sci. 2020 Nov 6;21(2):617-629. doi: 10.5114/aoms.2020.100649. eCollection 2025.

DOI:10.5114/aoms.2020.100649
PMID:40395886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12087322/
Abstract

INTRODUCTION

The present study examined the effects and mechanisms underlying long non-coding RNA (lncRNA) UBE2R2-AS1 in diabetes-induced renal injury.

MATERIAL AND METHODS

High glucose was used to imitate diabetes-induced renal injury in a cell model. Cell apoptosis rate was measured using flow cytometry, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) concentrations were evaluated using ELISA, and relative protein expression and amount were measured using western blot (WB) analysis and immunofluorescence, respectively. Correlations between lncRNA UBE2R2-AS1, miRNA-877-3p and TLR4 were analysed using the luciferase reporter assay.

RESULTS

Cell apoptosis rate and TNF-α and IL-6 concentrations were significantly higher ( < 0.001) in the high glucose (model) group compared with those of the Control group (CG) group. Following shRNA knockdown of lncRNA UBE2R2-AS1, the cell apoptosis rate and TNF-α and IL-6 concentrations were significantly lower ( < 0.001, respectively) compared with those of the model group. However, under high-glucose conditions, shRNA knockdown of UBE2R2-AS1 and miRNA-877-3p significantly increased ( < 0.001) the cell apoptosis rate as well as TNF-α and IL-6 concentrations compared with the shRNA UBE2R2-AS1 knockdown group. WB and immunofluorescence analysis showed that toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor κB (p65) (NF-κB(p65)) pathway proteins were significantly stimulated in the model group compared with those in the CG, whereas shRNA transfection with miRNA-877-3p stimulation suppressed the TLR4/MyD88/NF-κB(p65) pathway.

CONCLUSIONS

Knockdown of lncRNA UBE2R2-AS1 improves diabetes-induced renal injury via regulation of the miRNA-877-3p/TLR4 axis .

摘要

引言

本研究探讨了长链非编码RNA（lncRNA）UBE2R2-AS1在糖尿病诱导的肾损伤中的作用及其机制。

材料与方法

在细胞模型中用高糖模拟糖尿病诱导的肾损伤。采用流式细胞术检测细胞凋亡率，用酶联免疫吸附测定（ELISA）评估肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）浓度，分别用蛋白质免疫印迹（WB）分析和免疫荧光法检测相关蛋白的表达和含量。用荧光素酶报告基因检测法分析lncRNA UBE2R2-AS1、miRNA-877-3p和Toll样受体4（TLR4）之间的相关性。

结果

与对照组（CG）相比，高糖（模型）组细胞凋亡率以及TNF-α和IL-6浓度显著更高（<0.001）。lncRNA UBE2R2-AS1经短发夹RNA（shRNA）敲低后，与模型组相比，细胞凋亡率以及TNF-α和IL-6浓度显著更低（分别为<0.001）。然而，在高糖条件下，与shRNA敲低UBE2R2-AS1组相比，shRNA敲低UBE2R2-AS1和miRNA-877-3p显著增加了（<0.001）细胞凋亡率以及TNF-α和IL-6浓度。WB和免疫荧光分析显示，与CG组相比，模型组中Toll样受体4（TLR4）/髓样分化因子88（MyD88）/核因子κB（p65）（NF-κB(p65)）信号通路蛋白受到显著激活，而转染shRNA并刺激miRNA-877-3p可抑制TLR4/MyD88/NF-κB(p65)信号通路。

结论

敲低lncRNA UBE2R2-AS1可通过调节miRNA-877-3p/TLR4轴改善糖尿病诱导的肾损伤。

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