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Overexpression of Mitochondrial Ferritin Sensitizes Cells to Oxidative Stress Via an Iron-Mediated Mechanism
Lu, ZB; Nie, GJ; Li, YY; Soe-Lin, S; Tao, Y; Cao, YL; Zhang, ZY; Liu, NQ; Ponka, P; Zhao, BL; Zhang ZY(张智勇); Liu NQ(刘年庆)
2009
发表期刊ANTIOXIDANTS & REDOX SIGNALING
卷号11期号:8页码:1791-1803
通讯作者[Soe-lin, Shan ; Ponka, Prem] McGill Univ, Lady Davis Inst Med Res, Sir Mortimer B Davis Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada ; [Soe-lin, Shan ; Ponka, Prem] McGill Univ, Dept Physiol, Montreal, PQ H3T 1E2, Canada ; [Ponka, Prem] McGill Univ, Dept Med, Montreal, PQ H3T 1E2, Canada ; [Zhang, Zhiyong ; Liu, Nianqing] Chinese Acad Sci, Inst High Energy Phys, Sychrotron Radiat Lab, Beijing, Peoples R China ; [Nie, Guangjun ; Li, Yiye] Chinese Acad Sci, Natl Ctr Nanosci & Technol China, Key Lab Biomed Effects Nanomat & Nanosafety, Beijing, Peoples R China ; [Lu, Zhongbing ; Tao, Yi ; Cao, Yuanlin ; Zhao, Baolu] Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Recognit Lab, Beijing, Peoples R China
文章类型Article
摘要Mitochondrial ferritin (MtFt) is a newly identified H-ferritin-like protein expressed only in mitochondria. Previous studies have shown that its overexpression markedly affects intracellular iron homeostasis and rescues defects caused by frataxin deficiency. To assess how MtFt exerts its function under oxidative stress conditions, MtFt overexpressing cells were treated with tert-butyl-hydroperoxide (tBHP), and the effects of MtFt expression on cell survival and iron homeostasis were examined. We found that MtFt expression was associated with decreased mitochondrial metabolic activity and reduced glutathione levels as well as a concomitant increase in reactive oxygen species levels and apoptosis. Moreover, mechanistic studies demonstrated that tBHP treatment led to a prolonged decrease in cytosolic ferritins levels in MtFt-expressing cells, while ferritin levels recovered to basal levels in control counterparts. tBHP treatment also resulted in elevated transferrin receptors, followed by more iron acquisition in MtFt expressing cells. The high molecular weight desferrioxamine, targeting to lysosomes, as well as the hydrophobic iron chelator salicylaldehyde isonicotinoyl hydrazone significantly attenuated tBHP-induced cell damage. In conclusion, the current study indicates that both the newly acquired iron from the extracellular environment and internal iron redistribution from ferritin degradation may be responsible for the increased sensitivity to oxidative stress in MtFt-expressing cells. Antioxid. Redox Signal. 11, 1791-1803.
学科领域Biochemistry & Molecular Biology; Endocrinology & Metabolism
DOI10.1089/ars.2008.2306
URL查看原文
语种英语
WOS研究方向Biochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS类目Biochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS记录号WOS:000267488900003
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文献类型期刊论文
条目标识符http://ir.ihep.ac.cn/handle/311005/239528
专题多学科研究中心
作者单位中国科学院高能物理研究所
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Lu, ZB,Nie, GJ,Li, YY,et al. Overexpression of Mitochondrial Ferritin Sensitizes Cells to Oxidative Stress Via an Iron-Mediated Mechanism[J]. ANTIOXIDANTS & REDOX SIGNALING,2009,11(8):1791-1803.
APA Lu, ZB.,Nie, GJ.,Li, YY.,Soe-Lin, S.,Tao, Y.,...&刘年庆.(2009).Overexpression of Mitochondrial Ferritin Sensitizes Cells to Oxidative Stress Via an Iron-Mediated Mechanism.ANTIOXIDANTS & REDOX SIGNALING,11(8),1791-1803.
MLA Lu, ZB,et al."Overexpression of Mitochondrial Ferritin Sensitizes Cells to Oxidative Stress Via an Iron-Mediated Mechanism".ANTIOXIDANTS & REDOX SIGNALING 11.8(2009):1791-1803.
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