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Poly(ADP-ribose) protects vascular smooth muscle cells from oxidative DNA damage
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  • Journal title : BMB Reports
  • Volume 48, Issue 6,  2015, pp.354-359
  • Publisher : Korean Society for Biochemistry and Molecular Biology
  • DOI : 10.5483/BMBRep.2015.48.6.012
 Title & Authors
Poly(ADP-ribose) protects vascular smooth muscle cells from oxidative DNA damage
Zhang, Chao; Luo, Tao; Cui, Shijun; Gu, Yongquan; Bian, Chunjing; Chen, Yibin; Yu, Xiaochun; Wang, Zhonggao;
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 Abstract
Vascular smooth muscle cells (VSMCs) undergo death during atherosclerosis, a widespread cardiovascular disease. Recent studies suggest that oxidative damage occurs in VSMCs and induces atherosclerosis. Here, we analyzed oxidative damage repair in VSMCs and found that VSMCs are hypersensitive to oxidative damage. Further analysis showed that oxidative damage repair in VSMCs is suppressed by a low level of poly (ADP-ribosyl)ation (PARylation), a key post-translational modification in oxidative damage repair. The low level of PARylation is not caused by the lack of PARP-1, the major poly(ADP-ribose) polymerase activated by oxidative damage. Instead, the expression of poly(ADP-ribose) glycohydrolase, PARG, the enzyme hydrolyzing poly(ADP-ribose), is significantly higher in VSMCs than that in the control cells. Using PARG inhibitor to suppress PARG activity facilitates oxidative damage-induced PARylation as well as DNA damage repair. Thus, our study demonstrates a novel molecular mechanism for oxidative damage-induced VSMCs death. This study also identifies the use of PARG inhibitors as a potential treatment for atherosclerosis. [BMB Reports 2015; 48(6): 354-359]
 Keywords
DNA damage;Oxidative stress;Poly(ADP-ribosyl)ation;Poly(ADP-ribose) glycohydrolase;Vascular smooth muscle cells;
 Language
English
 Cited by
1.
SIRT1 improves VSMC functions in atherosclerosis, Progress in Biophysics and Molecular Biology, 2016, 121, 1, 11  crossref(new windwow)
2.
Synergetic Effects of PARP Inhibitor AZD2281 and Cisplatin in Oral Squamous Cell Carcinoma in Vitro and in Vivo, International Journal of Molecular Sciences, 2016, 17, 3, 272  crossref(new windwow)
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