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MicroRNA-9-5p promotes angiogenesis but inhibits apoptosis and inflammation of high glucose-induced injury in human umbilical vascular endothelial cells by targeting CXCR4.

Authors :
Yi, Jun
Gao, Zhi-Feng
Source :
International Journal of Biological Macromolecules. Jun2019, Vol. 130, p1-9. 9p.
Publication Year :
2019

Abstract

High glucose (HG) has the potential to cause vascular endothelial cell injury, while microRNAs (miRNAs) play a key role in treating endothelial cell injury. CXC chemokine receptor-4 (CXCR4) is reported to be expressed in vascular endothelial cells. Hence, this study investigated role of miR-9-5p in the angiogenesis and apoptosis of HG-induced human umbilical vascular endothelial cells (HUVECs) injury. Dual luciferase reporter gene assay verified that miR-9-5p targeted CXCR4. RT-qPCR and western blot analysis revealed that miR-9-5p was down-regulated, meanwhile CXCR4 was up-regulated in the HG-induced HUVECs. HUVECs were cultured in 30 mmol/L HG in vitro, and then transfected with miR-9-5p mimic or CXCR4 siRNA to identify the effect of miR-9-5p on cell activity, angiogenesis, apoptosis, and inflammation of HG-induced HUVECs. The results suggested that overexpression of miR-9-5p or silencing of CXCR4 in HG-induced HUVECs increased cell proliferation and tubule length, while decreasing the apoptosis rate and the expression of inflammatory factors. Furthermore, miR-9-5p inhibited the phosphorylation of extracellular regulated protein kinases (ERK), protein kinase B (AKT), and Mammalian Target of Rapamycin (mTOR) proteins via downregulation of CXCR4. Therefore, overexpression of miR-9-5p suppressed the mitogen-activated protein kinase (MAPK)/ERK and the PI3K/AKT/mTOR pathway by inhibiting CXCR4, thereby reducing HG-induced injury in HUVECs. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01418130
Volume :
130
Database :
Academic Search Index
Journal :
International Journal of Biological Macromolecules
Publication Type :
Academic Journal
Accession number :
136344063
Full Text :
https://doi.org/10.1016/j.ijbiomac.2019.02.003