o8G-miR-6513-5p/BCL2L13 轴调控人隐静脉内皮细胞在氧化应激过程中的有丝分裂。

IF 3.2 3区 生物学 Q3 MATERIALS SCIENCE, BIOMATERIALS
Hao Jia, Le Kang, Ben Huang, Shuyang Lu, Zhiwen Ding, Zhenhang Chen, Chunsheng Wang, Jiangping Song, Yunzeng Zou, Yongxin Sun
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引用次数: 0

摘要

冠状动脉旁路移植术(CABG)中会出现静脉移植物衰竭(VGD),而手术过程中的缺血再灌注氧化应激损伤与 VGD 有关。为了探索这一过程中细胞表型的变化,我们构建了一个稳定的人隐静脉内皮细胞(HSVECs)氧化应激模型。通过蛋白质组学和细胞实验发现,BCL2L13在HSVECs氧化应激过程中表达上调,BCL2L13通过受体介导的与LC3的相互作用调控有丝分裂,并在细胞保护中发挥作用。在氧化应激过程中,细胞内发生了o8G表观遗传修饰,miR-6513-5p的o8G修饰使该分子失去了对BCL2L13的靶向调控作用,参与了BCL2L13的上调。当HSVECs发生氧化应激时,存在一条o8G修饰-BCL2L13-LC3-嗜丝虫吞噬的调控途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
o8G-miR-6513-5p/BCL2L13 Axis Regulates Mitophagy during Oxidative Stress in the Human Saphenous Vein Endothelial Cells.

Venous graft decay (VGD) occurs in coronary artery bypass grafting (CABG), and ischemia-reperfusion oxidative stress injury during the operation is involved in VGD. To explore the cellular phenotypic changes during this process, a stable oxidative stress model of human saphenous vein endothelial cells (HSVECs) is constructed. Through proteomics and cell experiments, it is found that the expression of BCL2L13 is upregulated during oxidative stress of HSVECs, and BCL2L13 regulated mitophagy through receptor-mediated interaction with LC3 and plays a role in cell protection. During oxidative stress, intracellular o8G epigenetic modification occurs, and the o8G modification of miR-6513-5p causes this molecule to lose its targeted regulation of BCL2L13 and participates in the upregulation of BCL2L13. There is a regulatory pathway of o8G modification-BCL2L13-LC3-mitophagy when oxidative stress occurs in HSVECs.

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来源期刊
Advanced biology
Advanced biology Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
6.60
自引率
0.00%
发文量
130
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