Overexpression of miR-223 reduces survival of human aortic endothelial cells with H<sub>2</sub>O<sub>2</sub>-induced oxidative stress <italic style="font-style: italic">in vitro</italic> by directly targeting PARP1

Jinyu MA; Kang JIANG; Tao FENG

doi:10.16016/j.1000-5404.201711201

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Overexpression of miR-223 reduces survival of human aortic endothelial cells with H₂O₂-induced oxidative stress in vitro by directly targeting PARP1

Basic Medicine | 更新时间：2026-01-09

- Overexpression of miR-223 reduces survival of human aortic endothelial cells with H₂O₂-induced oxidative stress in vitro by directly targeting PARP1
- Journal of Third Military Medical University Vol. 40, Issue 14, Pages: 1301-1305(2018)
- 作者机构：
  
  473000 河南南阳，南阳医学高等专科学校第一附属医院神经内科
- 作者简介：
- 基金信息：
- DOI：10.16016/j.1000-5404.201711201
  CLC： R322.121; R363.22; R394-3
- Received：23 November 2017，
  
  Revised：2018-04-21，
  
  Published：30 July 2018
- 稿件说明：
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Jinyu MA, Kang JIANG, Tao FENG. Overexpression of miR-223 reduces survival of human aortic endothelial cells with H₂O₂-induced oxidative stress in vitro by directly targeting PARP1[J]. Journal of Third Military Medical University, 2018, 40(14): 1301-1305.
DOI：

Jinyu MA, Kang JIANG, Tao FENG. Overexpression of miR-223 reduces survival of human aortic endothelial cells with H₂O₂-induced oxidative stress in vitro by directly targeting PARP1[J]. Journal of Third Military Medical University, 2018, 40(14): 1301-1305. DOI： 10.16016/j.1000-5404.201711201.

摘要

目的

探讨miR-223通过靶向PARP1对氧化应激状态下人主动脉内皮细胞HAECs存活的影响及miR-223改善氧化应激来治疗高血压的潜能。

方法

TargetScan预测靶向PARP1的潜在miRNAs；双荧光素酶报告实验检测miR-223对PARP1的靶向调节作用；qPCR和western blot检测miR-223对HAECs细胞中PARP1 mRNA和蛋白表达影响；用H

诱导人主动脉内皮细胞HAECs产生氧化应激，单细胞凝胶电泳、克隆形成实验和MTT分别检测miR-223对细胞DNA损伤、存活能力的影响。

结果

软件预测发现miR-223是PARP1的潜在miRNAs；双荧光素酶报告实验、qPCR及western blot均证实了miR-223对PARP1的靶向调控作用；过表达miR-223可通过降低PARP1表达促进H

诱导人主动脉内皮细胞HAECs氧化损伤，降低细胞存活能力。

结论

miR-223通过靶向调节PARP1表达降低H

诱导后人主动脉内皮细胞HAECs存活，有可能成为高血压治疗的新靶点。

Abstract

Objective

To investigate the effect of miR-223 overexpression on the survival of human aortic endothelial cells (HAECs) under oxidative stress and explore the underlying mechanism.

Methods

Targetscan was used to predict the potential miRNAs targeting poly-(ADP-ribose) polymerase 1 (PARP1). Dual luciferase reporter assay

qPCR and Western blotting were used to evaluate the effect of miR-223 overexpression on PARP1 in cultured HAECs transfected with miR-223 using Lipofectamine 2000. The effect of miR-223 overexpression on DNA damage and cell viability in HAECs exposed to H

-induced oxidative stress was investigated using single cell gel electrophoresis

clonogenic assay and MTT assay.

Results

Bioinformatics analysis indicated that PARP1 was a potential target of miR-223. The results of dual luciferase reporter assay

qPCR and Western blotting all supported the role of miR-223 for targeted modulation of PARP1 in HAECs. Overexpression of miR-223

obviously exacerbated oxidative cell damage and decreased the cell viability in HAECs exposed to H

Conclusion

The overexpression of miR-223 reduces the survival of cultured HAECs with H

-induced oxidative stress by targeting PARP1

suggesting the potential of miR-223 as a therapeutic target for improving hypertension induced by oxidative stress.

关键词

Keywords

references

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Overexpression of miR-223 reduces survival of human aortic endothelial cells with H2O2-induced oxidative stress in vitro by directly targeting PARP1

DOI：10.16016/j.1000-5404.201711201

摘要

Abstract

关键词

Keywords

references

Overexpression of miR-223 reduces survival of human aortic endothelial cells with H₂O₂-induced oxidative stress in vitro by directly targeting PARP1