Open AccessmiR-200c serves an important role in H5V endothelial cells in high glucose by targeting Notch1
Author(s) -
Yunfeng Zhang,
Qiang Guan,
Xing Jin
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.6792
Subject(s) - hes1 , microrna , transfection , biology , apoptosis , western blot , downregulation and upregulation , oncogene , endothelial stem cell , cancer research , cell cycle , microbiology and biotechnology , gene , in vitro , biochemistry
Diabetic vasculopathy is the leading cause of impairment and death in diabetic patients, a variety of factors are involved in its underlying pathological process, however, endothelial cell (EC) dysfunction serves a significant role in the process. MicroRNAs (miRNAs) have emerged as potential therapeutic candidates, due to their ability to regulate multiple targets involved in ECs. The aim of the present study was to investigate the role of miR‑200c in regulating ECs in high glucose condition. To investigate the role of miR‑200c in regulating hyperglycemia induced ECs by targeting Notch1, ECs H5V cells were cultured in high sugar conditions to initiate the inhibition of Notch1, the same cells in normal medium as the control. H5V cells were transfected with miR‑200c mimics, miR‑200c inhibitors or scrambled oligonucleotide controls, respectively. Notch1 and Hes1 mRNA and protein expression level were detected by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The present study reported that miR‑200c was highly expressed by high glucose stimulation in H5V cells, however Notch1 was inhi-bited by high glucose, and it was also depressed by miR‑200c in high glucose conditions. Notch1 was identified as the target gene of miR‑200c, luciferase reporter assays confirmed the biochemical relationship for miR‑200c decreasing Notch1. The current findings revealed that miR‑200c may inhibit Notch1 expression in high glucose conditions, which suggested that miR‑200c mediating Notch1/Hes1 may involve in the process of vascular damage caused by hyperglycemia.