miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

doi:10.1016/j.freeradbiomed.2016.01.005

CORC > 合肥物质科学研究院 > 中国科学院合肥物质科学研究院 > 中科院等离子体物理研究所

	miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2
	Gao, Ming 1; Liu, Yun 1,2; Chen, Yue 1,3; Yin, Chunyang 1; Chen, Jane-Jane 4; Liu, Sijin 1
刊名	FREE RADICAL BIOLOGY AND MEDICINE
	2016-03-01
卷号	92 期号:无页码:39-49
关键词	Mir-214 Nrf2 Atf4 Ezh2 Erythroid Cells
DOI	10.1016/j.freeradbiomed.2016.01.005
文献子类	Article
英文摘要	Nuclear factor (erythroid-derived 2) like 2 (Nrf2) is a key regulator in protecting cells against stress by targeting many anti-stress response genes. Recent evidence also reveals that Nrf2 functions partially by targeting mircroRNAs (miRNAs). However, the understanding of Nrf2-mediated cytoprotection through miRNA-dependent mechanisms is largely unknown. In the current study, we identified a direct Nrf2 targeting miRNA, miR-214, and demonstrated a protective role of miR-214 in erythroid cells against oxidative stresses generated by radiation, excess iron and arsenic (As) exposure. miR-214 expression was transcriptionally repressed by Nrf2 through a canonical antioxidant response element (ARE) within its promoter region, and this repression is ROS-dependence. The suppression of miR-214 by Nrf2 could antagonize oxidative stress-induced cell death in erythroid cells by two ways. First, miR-214 directly targeted ATF4, a crucial transcriptional factor involved in anti-stress responses, down regulation of miR-214 releases the repression of ATF4 translation and leads to increased ATF4 protein content. Second, miR-214 was able to prevent cell death by targeting EZH2, the catalytic core component of PRC2 complex that is responsible for tri-methylation reaction at lysine 27 (K27) of histone 3 (H3) (H3K27me3), by which As induced miR-214 reduction resulted in an increased global H3K27me3 level and a compromised over expression of a pro-apoptotic gene Bim. These two pathways downstream of miR-214 synergistically cooperated to antagonize erythroid cell death upon oxidative stress. Our combined data revealed a protective role of miR-214 signaling in erythroid cells against oxidative stress, and also shed new light on Nrf2-mediated cytoprotective machinery. (C) 2016 Elsevier Inc. All rights reserved.
WOS关键词	REGULATED EIF2-ALPHA KINASE ; HEME OXYGENASE-1 GENE ; SIGNALING PATHWAY ; ANTIOXIDANT RESPONSE ; STEM-CELLS ; NRF2 ; ERYTHROPOIESIS ; METABOLISM ; IRON ; TRANSCRIPTION
WOS研究方向	Biochemistry & Molecular Biology ; Endocrinology & Metabolism
语种	英语
WOS记录号	WOS:000370645400004
资助机构	National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; National "973" Program(2014CB932000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; Strategic Priority Research Program of the Chinese Academy of Sciences(XDB14000000) ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; National Natural Science Foundation of China(21507154 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21425731 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21377159 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21177151 ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152) ; 21207152)
内容类型	期刊论文
源URL	[http://ir.hfcas.ac.cn:8080/handle/334002/21829]
专题	合肥物质科学研究院_中科院等离子体物理研究所
作者单位	1.Chinese Acad Sci, Ecoenvironm Sci Res Ctr, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China 2.Chinese Acad Sci & Anhui Prov, Key Lab Ion Beam Bioengn, Hefei Inst Phys Sci, Hefei 230031, Anhui, Peoples R China 3.Tianjin Med Univ, Dept Urol, Hosp 2, Tianjin Inst Urol, Tianjin 300211, Peoples R China 4.MIT, Inst Med Engn & Sci, 77 Massachusetts Ave, Cambridge, MA 02139 USA
推荐引用方式 GB/T 7714	Gao, Ming,Liu, Yun,Chen, Yue,et al. miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2[J]. FREE RADICAL BIOLOGY AND MEDICINE,2016,92(无):39-49.
APA	Gao, Ming,Liu, Yun,Chen, Yue,Yin, Chunyang,Chen, Jane-Jane,&Liu, Sijin.(2016).miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2.FREE RADICAL BIOLOGY AND MEDICINE,92(无),39-49.
MLA	Gao, Ming,et al."miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2".FREE RADICAL BIOLOGY AND MEDICINE 92.无(2016):39-49.