Effect of MiR-200b on retinal endothelial cell function in high-glucose condition and the mechanism.
- Author:
Qun JIANG
1
;
Xiao-Hua ZHU
;
Xin-Min LIU
;
Jian-Ming LIU
Author Information
- Publication Type:Journal Article
- MeSH: Blotting, Western; Cell Proliferation; Cells, Cultured; Culture Media; chemistry; Diabetic Retinopathy; Endothelial Cells; cytology; Glucose; chemistry; Humans; MicroRNAs; metabolism; RNA, Messenger; Real-Time Polymerase Chain Reaction; Retina; cytology; Transfection; Transforming Growth Factor beta1; metabolism; Vascular Endothelial Growth Factor A; metabolism
- From: Journal of Southern Medical University 2016;36(4):577-581
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of MiR-200b on human retinal endothelial cells (hRECs) cultured in high glucose and explore the mechanism.
METHODShRECs cultured in high glucose or in normal media were examined for MiR-200b mRNA expression using real-time PCR. The effect of MiR-200b transfection on hREC proliferation in high-glucose culture was evaluated with MTT assay, and real-time PCR and Western blotting were performed to determine vascular endothelial growth factor (VEGF) and transforming growth factor β1 (TGFβ1) expression in the transfected cells.
RESULTSThe cells in high-glucose culture showed significantly decreased MiR-200b expression and active proliferation. Compared with those in normal control cells, VEGF and TGFβ1 mRNA and protein expressions increased markedly in cells cultured in high glucose (P<0.05). MiR-200b transfection of the cells caused significantly increased cellular expression of MiR-200b but decreased expression levels of VEGF and TGFβ1 mRNA and protein, and suppressed hREC proliferation in high glucose culture (P<0.05).
CONCLUSIONMiR-200b can regulate REC growth and proliferation by changing VEGF and TGFβ1 expressions and thus play a role in the pathogenesis and progression of diabetic retinopathy.
