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The Roles of p21(Waf1/CIP1) and Hus1 in Generation and Transmission of Damage Signals Stimulated by Low-Dose Alpha-Particle Irradiation

文献类型：期刊论文

作者Zhao, Ye1; Ma, Xiaoyan2,3; Wang, Jun1,4; Chen, Shaopeng1,4; Yuan, Hang1,4; Xu, An1,4; Hang, Haiying2,3; Wu, Lijun1,4,5
刊名RADIATION RESEARCH
出版日期2015-12-01
卷号184期号:6页码:578-585
DOI10.1667/RR4165.1
文献子类Article
英文摘要Previously reported studies have demonstrated the involvement of p21(Waf1/CIP1) in radiation-induced bystander effects (RIBE). Mouse embryonic fibroblasts (MEFs) lacking Hus1 fail to proliferate in vitro, but inactivation of p21 allows for the continued growth of Hus1-deficient cells, indicating the close connection between p21 and Hus1 cells. In this study, wildtype MEFs, Hus1(+/+)p21(-/-) MEFs and p21(-/-)Hus1(-/-) MEFs were used in a series of radiation-induced bystander effect experiments, the roles of p21 and Hus1 in the induction and transmission of radiation-induced damage signals were investigated. Our results showed that after 5 cGy alpha particle irradiation, wild-type MEFs induced significant increases in gamma-H2AX foci and micronuclei formation in bystander cells, whereas the bystander effects were not detectable in p21(-/-)Hus1(+/+) MEFs and were restored again in p21(-/-)Hus1(-/-) MEFs. Media transfer experiments showed that p21(-/-)Hus1(+/+) MEFs were deficient in the production bystander signals, but could respond to bystander signals. We further investigated the mitogen-activated protein kinases (MAPKs) that might be involved in the bystander effects. It was found that although knocking out p21 did not affect the expression of connexin43 and its phosphorylation, it did result in inactivation of some MAPK signal pathway kinases, including JNK1/2, ERK1/2 and p38, as well as a decrease in reactive oxygen species (ROS) levels in irradiated cells. However, the activation of MAPK kinases and the ROS levels in irradiated cells were restored in the cell line by knocking out Hus1. These results suggest that p21(Waf1/CIP1) and Hus1 play crucial roles in the generation and transmission of bystander damage signals after low-dose a particle irradiation. (C) 2015 by Radiation Research
WOS关键词DNA-DAMAGE ; INTERCELLULAR COMMUNICATION ; OXIDATIVE STRESS ; MAPK PATHWAYS ; MOUSE HUS1 ; CELL-CYCLE ; IN-VIVO ; BYSTANDER ; REPLICATION ; CHECKPOINT
WOS研究方向Life Sciences & Biomedicine - Other Topics ; Biophysics ; Radiology, Nuclear Medicine & Medical Imaging
语种英语
WOS记录号WOS:000367160700004
资助机构National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; National Natural Science Foundation of China(81273004 ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; CAS/SAFEA International Partnership Program for Creative Research Teams ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14030502) ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 30770504 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 31470829 ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009) ; 10935009)
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/30207]  
专题合肥物质科学研究院_技术生物与农业工程研究所
作者单位1.Chinese Acad Sci, Hefei Inst Phys Sci, Key Lab Ion Beam Bioengn, Hefei 230031, Anhui, Peoples R China
2.Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China
3.Chinese Acad Sci, Ctr Computat & Syst Biol, Beijing 100101, Peoples R China
4.Key Lab Environm Toxicol & Pollut Control Technol, Hefei 230031, Anhui, Peoples R China
5.Univ Sci & Technol China, Sch Nucl Sci & Technol, Hefei 230026, Anhui, Peoples R China
推荐引用方式
GB/T 7714		 Zhao, Ye,Ma, Xiaoyan,Wang, Jun,et al. The Roles of p21(Waf1/CIP1) and Hus1 in Generation and Transmission of Damage Signals Stimulated by Low-Dose Alpha-Particle Irradiation[J]. RADIATION RESEARCH,2015,184(6):578-585.
APA Zhao, Ye.,Ma, Xiaoyan.,Wang, Jun.,Chen, Shaopeng.,Yuan, Hang.,...&Wu, Lijun.(2015).The Roles of p21(Waf1/CIP1) and Hus1 in Generation and Transmission of Damage Signals Stimulated by Low-Dose Alpha-Particle Irradiation.RADIATION RESEARCH,184(6),578-585.
MLA Zhao, Ye,et al."The Roles of p21(Waf1/CIP1) and Hus1 in Generation and Transmission of Damage Signals Stimulated by Low-Dose Alpha-Particle Irradiation".RADIATION RESEARCH 184.6(2015):578-585.

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来源：合肥物质科学研究院

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