西安交通大学学报(医学版)2024,Vol.45Issue(5) :705-711.DOI:10.7652/jdyxb202405002

miR-26a-5p调控PTEN/PI3K/Akt信号通路对高糖诱导视网膜Müller细胞活化及凋亡的影响

Effects of miR-26a-5p on high glucose-induced retina Müller activation and apoptosis by regulating PTEN/PI3K/Akt signaling pathway

唐德荣 杨雨雯 石蕊 刘丹丹
西安交通大学学报(医学版)2024,Vol.45Issue(5) :705-711.DOI:10.7652/jdyxb202405002

miR-26a-5p调控PTEN/PI3K/Akt信号通路对高糖诱导视网膜Müller细胞活化及凋亡的影响

Effects of miR-26a-5p on high glucose-induced retina Müller activation and apoptosis by regulating PTEN/PI3K/Akt signaling pathway

唐德荣 1杨雨雯 2石蕊 3刘丹丹3
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作者信息

  • 1. 安康市职业技术学院医学院/安康市中心医院眼科,陕西安康 725000
  • 2. 温州医科大学,浙江温州 325035
  • 3. 陕西省人民医院眼科,陕西西安 710068
  • 折叠

摘要

目的 检测微小RNA-26a-5p(microRNA-26a-5p,miR-26a-5p)对PTEN/PI3K/Akt信号通路及高糖刺激的视网膜Müller细胞凋亡的影响,探讨糖尿病视网膜神经损伤的潜在机制.方法 采用不同浓度的葡萄糖刺激视网膜Müller细胞构建糖尿病视网膜神经损伤模型,采用CCK-8及流式细胞仪观察细胞增殖及凋亡情况,细胞转染过表达miR-26a-5p 模拟物,Real-time PCR 检测 miR-26a-5p、PTEN、PI3K、Akt 的表达情况,ELISA 测定细胞上清液中 IL-1β及IL-6的水平,采用Graphpad 8.0软件处理数据.结果 高糖刺激视网膜Müller细胞生长活跃,与对照组相比,50 mmol/L高糖刺激Müller细胞活力在12 h、24 h时逐渐增加,48 h时活力减弱,细胞凋亡增加,组间差异有统计学意义(P<0.05).高糖刺激后视网膜Müller细胞中miR-26a-5p水平下降,PTEN的表达显著升高,PI3K及Akt水平下降,IL-1β及IL-6的水平明显升高,过表达miR-26a-5p后,PTEN水平降低,PI3K/Akt及炎性因子降低,细胞凋亡减少(P<0.01).结论 miR-26a-5p通过调控PTEN/PI3K/Akt的表达,影响炎症因子释放,减轻高糖诱导的视网膜Müller细胞凋亡.

Abstract

Objective To investigate the effects of microRNA-26a-5p(miR-26a-5p)on high glucose-induced retina Müller activation and apoptosis by regulating PTEN/PI3K/Akt signaling pathway,and the potential mechanism of diabetic retinal neurodegeneration.Methods Various concentrations of high glucose were added into rMC-1 culture.CCK-8 and flow cytometry was used to examine cell proliferation and apoptosis respectively.The regulatory effects of miR-26a-5p on the expressions of PTEN,PI3K and Akt were observed by real-time PCR;the expression levels of IL-1β and IL-6 in Müller cells were examined by ELISA.The data were processed by Graphpad 8.0 software.Results Müller cells grew actively in high-glucose stimulation culture.Compared with the control group,the activity of Müller cells stimulated by 50 mmol/L glucose increased gradually at 12 h and 24 h,but decreased at 48 h after stimulation,when Müller cells apoptosis increased.The difference between the groups was statistically significant(P<0.05).The expression of miRNA-26a-5p decreased,that of PTEN increased,and those of PI3K and Akt decreased.Meanwhile,IL-1β and IL-6 levels were significantly increased in Müller cells.miR-26a-5p over-expression alleviated injuries to high glucose stimulated retinal Müller cells by inhibiting PTEN,which upregulated the expression of PI3K/Akt and downregulation of IL-1β and IL-6(P<0.01).Conclusion Upregulating miR-26a-5p protects Müller cells against apoptosis,probably through regulation of PTEN/PI3K/Akt and affecting the production of inflammatory factors.

关键词

视网膜Müller细胞/微小RNA-26a-5p(miR-26a-5p)/PTEN/PI3K/Akt/炎症/糖尿病视网膜病变

Key words

retinal Müller cell/microRNA-26a-5p(miR-26a-5p)/PTEN/PI3K/Akt/inflammation/diabetic retinopathy

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基金项目

陕西省自然科学基础研究计划项目(2022JM-571)

陕西省人民医院科技发展孵化基金资助项目(2021YJY-20)

出版年

2024
西安交通大学学报(医学版)
西安交通大学

西安交通大学学报(医学版)

CSTPCD北大核心
影响因子:1.144
ISSN:1671-8259
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