Overexpression of Mitochondrial Ferritin Sensitizes Cells to Oxidative Stress Via an Iron-Mediated Mechanism
文献类型:期刊论文
作者 | Lu, ZB; Nie, GJ; Li, YY; Soe-Lin, S; Tao, Y![]() |
刊名 | ANTIOXIDANTS & REDOX SIGNALING
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出版日期 | 2009 |
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 |
英文摘要 | 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. |
学科主题 | Biochemistry & Molecular Biology; Endocrinology & Metabolism |
类目[WOS] | Biochemistry & Molecular Biology ; Endocrinology & Metabolism |
研究领域[WOS] | Biochemistry & Molecular Biology ; Endocrinology & Metabolism |
原文出处 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000267488900003 |
源URL | [http://ir.ihep.ac.cn/handle/311005/239528] ![]() |
专题 | 高能物理研究所_多学科研究中心 |
作者单位 | 中国科学院高能物理研究所 |
推荐引用方式 GB/T 7714 | 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. |
入库方式: OAI收割
来源:高能物理研究所
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