MiR-429 Inhibits the Angiogenesis of Human Brain Microvascular Endothelial Cells through SNAI2-Mediated GSK-3ß/ß-Catenin Pathway.
Comput Math Methods Med
; 2021: 6753926, 2021.
Article
in En
| MEDLINE
| ID: mdl-34966442
ABSTRACT
MicroRNA (miRNA) dysfunction has been confirmed as a key event of ischemic stroke appearance. This study is aimed at revealing the role of miR-429 in the angiogenesis of HBMECs. The HBMECs were treated with oxygen and glucose deprivation (OGD) to establish the ischemic cell model. The qRT-PCR was used to measure the expression levels of the miR-429 in the serums of the patients or cells, and CCK-8, wound healing assay, and tube formation assay were used to observe the effects of miR-429 on the phenotype of HBMECs. Moreover, the Targetscan, dual-luciferase reporter assay, and Western blot were used to reveal the downstream target and regulation mechanism of miR-429 in OGD-induced HBMECs. The results showed that miR-429 was significantly upregulated in the serums of the patients, and overexpressed miR-429 could extremely inhibit the viability, migration, and tube formation of OGD-induced HBMECs. Furthermore, it was found that SNAI2 was a downstream factor of miR-429, and SNAI2 could rescue the effects of miR-429 on OGD-induced HBMECs. Besides, the Western blot showed that miR-429 could affect the activity of GSK-3ß/ß-catenin pathway via inhibiting the expression of SNAI2. In conclusion, this study suggests that miR-429 inhibits the angiogenesis of HBMECs through SNAI2-mediated GSK-3ß/ß-catenin pathway.
Full text:
1
Collection:
01-internacional
Health context:
1_ASSA2030
/
2_ODS3
Database:
MEDLINE
Main subject:
Brain
/
MicroRNAs
/
Beta Catenin
/
Glycogen Synthase Kinase 3 beta
/
Snail Family Transcription Factors
/
Neovascularization, Pathologic
Type of study:
Prognostic_studies
Limits:
Humans
Language:
En
Journal:
Comput Math Methods Med
Year:
2021
Document type:
Article