-
Something wrong with this record ?
PARP-1 Involvement in Autophagy and Their Roles in Apoptosis of Vascular Smooth Muscle Cells under Oxidative Stress
Y. Y. Meng, C. W. Wu, B. Yu, H. Li, M. Chen, G. X. Qi,
Language English Country Czech Republic
Document type Journal Article
NLK
Free Medical Journals
from 2000
Freely Accessible Science Journals
from 2000
ProQuest Central
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 2000
- MeSH
- Apoptosis * drug effects MeSH
- Autophagy * drug effects MeSH
- Caspases metabolism MeSH
- Myocytes, Smooth Muscle drug effects metabolism pathology MeSH
- Mice, Inbred C57BL MeSH
- Oxidative Stress * drug effects MeSH
- Hydrogen Peroxide toxicity MeSH
- Poly(ADP-ribose) Polymerases metabolism MeSH
- Muscle, Smooth, Vascular pathology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
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.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc19005387
- 003
- CZ-PrNML
- 005
- 20190221142126.0
- 007
- ta
- 008
- 190205s2018 xr ad f 000 0|eng||
- 009
- AR
- 024 __
- $a 10.14712/fb2018064030103 $2 doi
- 035 __
- $a (PubMed)30394268
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Meng, Y. Y. $u Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
- 245 10
- $a PARP-1 Involvement in Autophagy and Their Roles in Apoptosis of Vascular Smooth Muscle Cells under Oxidative Stress / $c Y. Y. Meng, C. W. Wu, B. Yu, H. Li, M. Chen, G. X. Qi,
- 520 9_
- $a 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.
- 650 _2
- $a zvířata $7 D000818
- 650 12
- $a apoptóza $x účinky léků $7 D017209
- 650 12
- $a autofagie $x účinky léků $7 D001343
- 650 _2
- $a kaspasy $x metabolismus $7 D020169
- 650 _2
- $a peroxid vodíku $x toxicita $7 D006861
- 650 _2
- $a myši inbrední C57BL $7 D008810
- 650 _2
- $a svaly hladké cévní $x patologie $7 D009131
- 650 _2
- $a myocyty hladké svaloviny $x účinky léků $x metabolismus $x patologie $7 D032389
- 650 12
- $a oxidační stres $x účinky léků $7 D018384
- 650 _2
- $a poly(ADP-ribosa)polymerasy $x metabolismus $7 D011065
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Wu, C. W. $u Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
- 700 1_
- $a Yu, B. $u Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China; The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin, Heilongjiang Province, China.
- 700 1_
- $a Li, H. $u Department of Cardiology, No.1 Central Hospital of Baoding, Baoding, Hebei Province, China
- 700 1_
- $a Chen, M. $u Department of Geriatrics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
- 700 1_
- $a Qi, G. X. $u Department of Geriatrics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
- 773 0_
- $w MED00011004 $t Folia biologica $x 0015-5500 $g Roč. 64, č. 3 (2018), s. 103-111
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/30394268 $y Pubmed
- 856 41
- $u https://fb.cuni.cz/file/5874/fb2018a0014.pdf $y plný text volně přístupný
- 910 __
- $a ABA008 $b A 970 $c 89 $y 4 $z 0
- 990 __
- $a 20190205 $b ABA008
- 991 __
- $a 20190220144148 $b ABA008
- 999 __
- $a ok $b bmc $g 1378277 $s 1043592
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2018 $b 64 $c 3 $d 103-111 $i 0015-5500 $m Folia biologica (Praha) $n Folia biol. (Praha) $x MED00011004
- LZP __
- $b NLK118 $a Pubmed-20190205