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Neuroprotective mechanism of mitochondrial ferritin on 6-hydroxydopamine-induced dopaminergic cell damage: implication for neuroprotection in parkinson's disease

文献类型:期刊论文

作者Shi, Zhen-Hua1,2; Nie, Guangjun3; Duan, Xiang-Lin1; Rouault, Tracey4; Wu, Wen-Shuang1; Ning, Bo3; Zhang, Nan1; Chang, Yan-Zhong1; Zhao, Bao-Lu2
刊名Antioxidants & redox signaling
出版日期2010-09-01
卷号13期号:6页码:783-796
ISSN号1523-0864
DOI10.1089/ars.2009.3018
通讯作者Chang, yan-zhong(frankyzchang@yahoo.com.hk)
英文摘要Neuronal iron homeostasis disruption and oxidative stress are closely related to the pathogenesis of parkinson's disease (pd). adult iron-regulatory protein 2 knockout (ireb2(-/-)) mice develop iron accumulation in white matter tracts and nuclei in different brain area and display severe neurodegeneration in purkinje cells of the cerebrum. mitochondrial ferritin (mtft), a newly discovered ferritin, specifically expresses in high energy-consuming cells, including neurons of brain and spinal cord. interestingly, the decreased expression of mtft in cerebrum, but not in striatum, matches the differential neurodegeneration pattern in these ireb2(-/-) mice. to explore its effect on neurodegeneration, the effects of mtft expression on 6-hydrodopamine (6-ohda)-induced neuronal damage was examined. the overexpression of mtft led to a cytosolic iron deficiency in the neuronal cells and significantly prevented the alteration of iron redistribution induced by 6-ohda. importantly, mtft strongly inhibited mitochondrial damage, decreased production of the reactive oxygen species and lipid peroxidation, and dramatically rescued apoptosis by regulating bcl-2, bax and caspase-3 pathways. in conclusion, this study demonstrates that mtft plays an important role in preventing neuronal damage in an 6-ohda-induced parkinsonian phenotype by maintaining iron homeostasis. regulation of mtft expression in neuronal cells may provide a new neuroprotective strategy for pd. antioxid. redox signal. 13, 783-796.
WOS关键词GREEN TEA POLYPHENOLS ; ENDOPLASMIC-RETICULUM STRESS ; NEUROBLASTOMA SH-SY5Y CELLS ; CENTRAL-NERVOUS-SYSTEM ; LABILE IRON POOL ; ROS-NO PATHWAY ; OXIDATIVE STRESS ; COMPLEX-I ; NEURODEGENERATIVE DISORDERS ; INDUCED NEUROTOXICITY
WOS研究方向Biochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS类目Biochemistry & Molecular Biology ; Endocrinology & Metabolism
语种英语
出版者MARY ANN LIEBERT, INC
WOS记录号WOS:000280119800006
URI标识http://www.irgrid.ac.cn/handle/1471x/2176027
专题高能物理研究所
通讯作者Chang, Yan-Zhong
作者单位1.Hebei Normal Univ, Coll Life Sci, Lab Mol Iron Metab, Shijiazhuang 050016, Hebei, Peoples R China
2.Acad Sinica, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100080, Peoples R China
3.Natl Ctr Nanosci & Technol China, CAS Key Lab Biol Effects Nanomat & Nanosafety, Beijing, Peoples R China
4.NICHHD, Program Mol Med, NIH, Bethesda, MD 20892 USA
推荐引用方式
GB/T 7714
Shi, Zhen-Hua,Nie, Guangjun,Duan, Xiang-Lin,et al. Neuroprotective mechanism of mitochondrial ferritin on 6-hydroxydopamine-induced dopaminergic cell damage: implication for neuroprotection in parkinson's disease[J]. Antioxidants & redox signaling,2010,13(6):783-796.
APA Shi, Zhen-Hua.,Nie, Guangjun.,Duan, Xiang-Lin.,Rouault, Tracey.,Wu, Wen-Shuang.,...&Zhao, Bao-Lu.(2010).Neuroprotective mechanism of mitochondrial ferritin on 6-hydroxydopamine-induced dopaminergic cell damage: implication for neuroprotection in parkinson's disease.Antioxidants & redox signaling,13(6),783-796.
MLA Shi, Zhen-Hua,et al."Neuroprotective mechanism of mitochondrial ferritin on 6-hydroxydopamine-induced dopaminergic cell damage: implication for neuroprotection in parkinson's disease".Antioxidants & redox signaling 13.6(2010):783-796.

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