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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.
- 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