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RUNX1 can mediate the glucose and O-GlcNAc-driven proliferation and migration of human retinal microvascular endothelial cells
BMJ Open Diabetes Research & Care ( IF 4.1 ) Pub Date : 2021-08-01 , DOI: 10.1136/bmjdrc-2020-001898
Xindan Xing 1, 2, 3, 4, 5 , Hanying Wang 1, 2, 3, 4, 5 , Tian Niu 1, 2, 3, 4, 5 , Yan Jiang 1, 2, 3, 4, 5 , Xin Shi 1, 2, 3, 4, 5 , Kun Liu 2, 3, 4, 5, 6
Affiliation  

Introduction This study aims to determine whether high glucose condition and dynamic O-linked N-acetylglucosamine (O-GlcNAc) modification can promote the proliferation and migration of human retinal microvascular endothelial cells (HRMECs) and whether Runt-related transcription factor 1 (RUNX1) could mediate the glucose and O-GlcNAc-driven proliferation and migration of HRMECs. Research design and methods Western blot analysis was used to detect the O-GlcNAc modification level and RUNX1 level in cells and retina tissues, cell growth was studied by cell counting kit-8 assay, cell proliferation was detected by immunofluorescence staining. Then, cell migration and tube formation were investigated by scratch-wound assay, Transwell assay, and tube-forming assay. The changes of retinal structure were detected by H&E staining. The O-GlcNAc modification of RUNX1 was detected by immunoprecipitation. Results High glucose increases pan-cellular O-GlcNAc modification and the proliferation and migration of HRMECs. Hence, O-GlcNAc modification is critical for the proliferation and migration of HRMECs. RUNX1 mediates the glucose and O-GlcNAc-driven proliferation and migration in HRMECs. RUNX1 can be modified by O-GlcNAc, and that the modification is enhanced in a high glucose environment. Conclusions The present study reveals that high glucose condition directly affects retinal endothelial cells (EC) function, and O-GlcNAc modification is critical for the proliferation and migration of HRMECs, RUNX1 may take part in this mechanism, and maybe the function of RUNX1 is related to its O-GlcNAc modification level, which provides a new perspective for studying the mechanism of RUNX1 in diabetic retinopathy. All data relevant to the study are included in the article.

中文翻译:

RUNX1可介导葡萄糖和O-GlcNAc驱动的人视网膜微血管内皮细胞增殖和迁移

引言 本研究旨在确定高糖条件和动态 O-连接 N-乙酰氨基葡萄糖 (O-GlcNAc) 修饰是否可以促进人视网膜微血管内皮细胞 (HRMECs) 的增殖和迁移,以及 Runt 相关转录因子 1 (RUNX1)可以介导葡萄糖和 O-GlcNAc 驱动的 HRMEC 增殖和迁移。研究设计与方法Western blot分析检测细胞和视网膜组织中O-GlcNAc修饰水平和RUNX1水平,细胞计数kit-8法检测细胞生长情况,免疫荧光染色检测细胞增殖情况。然后,通过划痕试验、Transwell 试验和管形成试验研究细胞迁移和管形成。H&E染色检测视网膜结构的变化。通过免疫沉淀检测 RUNX1 的 O-GlcNAc 修饰。结果高糖增加泛细胞O-GlcNAc修饰和HRMECs的增殖和迁移。因此,O-GlcNAc 修饰对于 HRMEC 的增殖和迁移至关重要。RUNX1 介导 HRMEC 中葡萄糖和 O-GlcNAc 驱动的增殖和迁移。RUNX1 可以通过 O-GlcNAc 进行修饰,并且该修饰在高葡萄糖环境中得到增强。结至其 O-GlcNAc 修饰水平,为研究RUNX1在糖尿病视网膜病变中的作用机制提供了新的视角。所有与研究相关的数据都包含在文章中。
更新日期:2021-08-04
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