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学科主题临床医学
Cobalt Protoporphyrin Induces HO-1 Expression Mediated Partially by FOXO1 and Reduces Mitochondria-Derived Reactive Oxygen Species Production
Liu, Xiaojun1,2; Cui, Ying1,2; Li, Meixia3; Xu, Haifeng4; Zuo, Jin1,2; Fang, Fude1,2; Chang, Yongsheng1,2
刊名PLOS ONE
2013-11-08
DOI10.1371/journal.pone.0080521
8期:11
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
资助者Major State Basic Research Development Program of China (973 Program) ; National Natural Science Foundation of China ; Major State Basic Research Development Program of China (973 Program) ; National Natural Science Foundation of China
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]HEME OXYGENASE-1 ; OXIDATIVE STRESS ; TRANSCRIPTION FACTORS ; SIGNALING PATHWAY ; CYTOCHROME-C ; FORKHEAD BOX ; BETA-CELLS ; ACTIVATION ; MECHANISM ; APOPTOSIS
英文摘要

Background: Reactive oxygen species arise in the mitochondria as byproducts of respiration and oxidase activity and have important roles in many physiological and pathophysiological conditions. The level of reactive oxygen species is regulated by a number of enzymes and physiological antioxidants, including HO-1, Sod2, catalase and COX-2, etc. And HO-1 against oxidative stress requires an increase in stress-responsive genes, such as Sod2 and catalase. Especially for the activity of HO-1, cobalt protoporphyrin is known to be a potent and effective inducer in many tissues. The transcription factor, FOXO1 is resistant to oxidative stress through downregulating reactive oxygen species production. Previous study showed that FOXO1 induces HO-1 expression by binding to HO-1 promoter. The question whether cobalt protoporphyrin induces HO-1 expression mediated by FOXO1 and subsequently lessens reactive oxygen species production remains to be elucidated.

Results: Cobalt protoporphyrin enhances the expression of FOXO1 and facilitates FOXO1 binding to HO-1 promoter and increasing its transcriptional activity without influencing the FOXO1 protein stability. CoPP induces HO-1 and other oxidative stress-responsive genes expression, such as catalase, cytochrome c, Sod2, and COX-2, and decreases mitochondria-derived reactive oxygen species production, which are mediated partially by FOXO1.

Conclusions: Cobalt protoporphyrin induces HO-1 and other oxidative stress-responsive genes expression mediated partially by FOXO1, and has an important role in reducing cellular reactive oxygen species level. Cobalt protoporphyrin may be a more promising therapeutic agent to upregulate some antioxidantive genes.

语种英语
所属项目编号2012CB517504 ; 81170763 ; 81100608 ; 31371191
资助者Major State Basic Research Development Program of China (973 Program) ; National Natural Science Foundation of China ; Major State Basic Research Development Program of China (973 Program) ; National Natural Science Foundation of China
WOS记录号WOS:000327216200113
Citation statistics
Cited Times:1[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62459
Collection北京大学临床肿瘤学院_介入治疗科
作者单位1.Chinese Acad Med Sci, Inst Basic Med Sci, Natl Lab Med Mol Biol, Beijing 100730, Peoples R China
2.Peking Union Med Coll, Beijing 100021, Peoples R China
3.Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100080, Peoples R China
4.Peking Univ, Canc Hosp & Inst, Dept Intervent Therapy, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100871, Peoples R China
Recommended Citation
GB/T 7714
Liu, Xiaojun,Cui, Ying,Li, Meixia,et al. Cobalt Protoporphyrin Induces HO-1 Expression Mediated Partially by FOXO1 and Reduces Mitochondria-Derived Reactive Oxygen Species Production[J]. PLOS ONE,2013,8(11).
APA Liu, Xiaojun.,Cui, Ying.,Li, Meixia.,Xu, Haifeng.,Zuo, Jin.,...&Chang, Yongsheng.(2013).Cobalt Protoporphyrin Induces HO-1 Expression Mediated Partially by FOXO1 and Reduces Mitochondria-Derived Reactive Oxygen Species Production.PLOS ONE,8(11).
MLA Liu, Xiaojun,et al."Cobalt Protoporphyrin Induces HO-1 Expression Mediated Partially by FOXO1 and Reduces Mitochondria-Derived Reactive Oxygen Species Production".PLOS ONE 8.11(2013).
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