scholarly journals DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway

2018 ◽  
Vol 25 (3) ◽  
pp. 323-332 ◽  
Author(s):  
Dong‐Hua Mi ◽  
Hong‐Juan Fang ◽  
Guang‐Hui Zheng ◽  
Xian‐Hong Liang ◽  
Ya‐Rong Ding ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Rat Brain ◽  
High Glucose ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Vegf Pathway ◽  
Microvascular Endothelial ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals RUNX1 can mediate the glucose and O-GlcNAc-driven proliferation and migration of human retinal microvascular endothelial cells

2021 ◽  
Vol 9 (1) ◽  
pp. e001898
Author(s):  
Xindan Xing ◽  
Hanying Wang ◽  
Tian Niu ◽  
Yan Jiang ◽  
Xin Shi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Tube Formation ◽  
Cell Counting ◽  
Microvascular Endothelial Cells ◽  
High Glucose Condition ◽  
Microvascular Endothelial ◽  
And Migration ◽  
Glucose Condition ◽  
Proliferation And Migration

IntroductionThis 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 methodsWestern 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.ResultsHigh 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.ConclusionsThe 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.

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