BASIC RESEARCH
Vitamin D ameliorated endothelial cell damage induced by diabetes via regulation of lncRNA MEG3 in human umbilical vein endothelial cells
Hua Wei 1,   Qiongfang Zhang 2,   Jun Li 1,   Jing Yang 3,   Bin Huang 1,   Chun-chun Huang 1,   Ying-chuan Wang 4,   Jing-qian Hu 4,   Xi Wei 3
 
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1
Department of General Medicine, Affiliated Hospital of YouJiang Medical University for Nationalities, Baise, Guangxi, China
2
Department of General Medicine, The second NanNing people’s hospital, NanNing Guangxi, China
3
Health Supervision Center, Affiliated Hospital of YouJiang Medical University for Nationalities, Baise, Guangxi, China
4
Graduate School, YouJiang Medical University for Nationalities, Baise, Guangxi, China
Submission date: 2020-07-29
Final revision date: 2020-09-26
Acceptance date: 2020-10-01
Online publication date: 2020-11-25
 
 
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ABSTRACT
Introduction:
The purpose of this study was to investigate long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) effects in vitamin D (Vit. D) treatment in endothelial cell damage induced by diabetes.

Material and methods:
We used human umbilical vein endothelial cells (HUVECs) as a research objective in our study and used high glucose in a diabetic cell model. We evaluated cell apoptosis by flow cytometry, inflammatory factors (IL-6, IL-1β and TNF-α) concentrations by ELISA assay, relative gene and protein expression by RT-qPCR and WB assay, and NF-κB(p65) nuclear volume by cellular immunofluorescence.

Results:
Compared with the NC (normal control) group, the cell apoptosis rate was significantly increased, inflammatory factor (IL-6, IL-1β and TNF-α) concentrations were significantly up-regulated, lncRNA MEG3 gene expression was significantly depressed, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor B p65 (NF-κB(p65)) gene and protein expression levels were significantly increased and NF-κB(p65) nuclear volume was significantly up-regulated (p < 0.001, respectively). With Vit. D supplementation, compared with the Model group, Vit. D improved endothelial cell damage induced by diabetes, while lncRNA MEG3 was significantly increased and the TLR4/MyD88/NF-κB(p65) pathway was significantly depressed dose-dependently (all p < 0.05). With sh-MEG3 transfection, the Vit. D treatment effects were significantly reduced.

Conclusions:
Vit. D improved endothelial cell damage induced by diabetes via lncRNA MEG3 up-regulation in vitro study.

eISSN:1896-9151
ISSN:1734-1922