PARP-1 Involvement in Autophagy and Their Roles in Apoptosis of Vascular Smooth Muscle Cells under Oxidative Stress

Meng, Y. Y.; Wu, C. W.; Yu, B.; Li, H.; Chen, M.; Qi, Guoxian

doi:10.14712/fb2018064030103

Folia Biologica > Archive > 2018, Vol. 64 > Issue 3 > PARP-1 Involvement in Autophagy and…

Fol. Biol. 2018, 64, 103-111

https://doi.org/10.14712/fb2018064030103

PARP-1 Involvement in Autophagy and Their Roles in Apoptosis of Vascular Smooth Muscle Cells under Oxidative Stress

Y. Y. Meng¹, C. W. Wu¹, B. Yu^2,3, H. Li⁴, M. Chen⁵, Guoxian Qi⁵

¹Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
²Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China
³The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin, Heilongjiang Province, China
⁴Department of Cardiology, No.1 Central Hospital of Baoding, Baoding, Hebei Province, China
⁵Department of Geriatrics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China

Received April 2018
Accepted July 2018

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 explored 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.