These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: MicroRNA-9-5p promotes angiogenesis but inhibits apoptosis and inflammation of high glucose-induced injury in human umbilical vascular endothelial cells by targeting CXCR4.
    Author: Yi J, Gao ZF.
    Journal: Int J Biol Macromol; 2019 Jun 01; 130():1-9. PubMed ID: 30716366.
    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] [Full Text] [Related] [New Search]