Role of Bcl-2 family of proteins in mediating apoptotic death of PC12 cells exposed to oxygen and glucose deprivation

2005 ◽  
Vol 46 (1) ◽  
pp. 73-81 ◽  
Author(s):  
D KOUBI ◽  
H JIANG ◽  
L ZHANG ◽  
W TANG ◽  
J KUO ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Apoptotic Death

Postconditioning mitigates cell death following oxygen and glucose deprivation in PC12 cells and forebrain reperfusion injury in rats

2014 ◽  
Vol 93 (1) ◽  
pp. 140-148 ◽  
Author(s):  
Han-Chen Lin ◽  
Purnima Narasimhan ◽  
Shin-Yun Liu ◽  
Pak H. Chan ◽  
I-Rue Lai
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation

scholarly journals MiR-429 Inhibits the Angiogenesis of Human Brain Microvascular Endothelial Cells through SNAI2-Mediated GSK-3β/β-Catenin Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yameng Sun ◽  
Shenghao Ding ◽  
Yiling Fan ◽  
Fei Shen ◽  
Qing Dong ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Model ◽  
Glucose Deprivation ◽  
Tube Formation ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Oxygen And Glucose Deprivation ◽  
Downstream Target ◽  
Gsk 3Β

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-3β/β-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-3β/β-catenin pathway.

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