PARP-1 involvement in autopphagy and their roles in apoptosis of vascular smooth muscle cells under oxidative stress

Title:

PARP-1 involvement in autopphagy and their roles in apoptosis of vascular smooth muscle cells under oxidative stress

Creator:

Meng, Y. Y., Wu, C. W., Yu, B., Li, H., Chen, M, and Qi, G. X.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:12435ec9-a7c1-456f-8179-bda0e3de5750
uuid:12435ec9-a7c1-456f-8179-bda0e3de5750

Subject:

PARP-1, autophagy, AMPK-mTOR, oxidative stress, and apoptosis

Type:

model:article and TEXT

Format:

bez média and svazek

Description:

Autophagy and poly(ADP-ribose) polymerase 1 (PARP-1) are activated and involved in a series of cell processes under oxidative stress, which is associated with pathogenesis of atherosclerosis. Research on their relationship under oxidative stress has been limited. In this study, we aimed to investigate the activation, relationship, and role of autophagy and PARP-1 in vascular smooth muscle cell (VSMC) death under oxidative stress. This study ex-plored the signal molecule PARP-1 and autophagy in VSMCs using gene silencing and the hydrogen peroxide (H2O2)-stimulated oxidative stress model. We observed that H2O2 could induce autophagy in VSMCs, and the inhibition of autophagy could protect VSMCs against oxidative stress-mediated cell death. Meanwhile, PARP-1 could also be activated by H2O2. Additionally, we analysed the regulatory role of PARP-1 in oxidative stress-mediated autophagy and found that PARP-1 was a novel factor involved in the H2O2-induced autophagy via the AMPK-mTOR pathway. Finally, PARP-1 inhibition protected VSMCs against caspase-dependent apoptosis. These data suggested that PARP-1 played a critical role in H2O2-mediated autophagy and both of them were involved in apoptosis of VSMCs. and Corresponding author: Guoxian Qi

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Coverage:

[103]-111

Source:

Folia biologica | 2018 Volume:64 | Number:3

Harvested from:

CDK

Metadata only:

false