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α-synuclein在体外培养SH-SY5Y细胞中过表达致自体吞噬 被引量：1

Overexpression ofα-synuclein leads to autophagy in SH-SY5Y cells in vitro
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摘要 目的:观察α-synuclein转基因细胞内α-synuclein过表达对细胞超微结构的影响。方法:Lipofectamine法转染SHSY5Y细胞,用G418对转基因细胞进行筛选,免疫荧光细胞化学检测α-synuclein表达,电子显微镜观察转基因细胞超微结构的改变。结果:转基因细胞内出现大小不等、边界明显的自体吞噬体并伴有线粒体结构紊乱。结论:α-synuclein过表达可致细胞出现自体吞噬现象。 Objective: To observe the influence of overexpression of α-synuclein on the ultrastructure of culturedSH-SY5Y cells. Methods: The plasmid of α-synuclein-pcDNA3 was transfected into SH-SY5Y cells with lipofectamine. The expression of α-synuclein was determined by anti-α-synuclein immunocytochemistry. Ultrastructural alterations in the transfected cells were determined with electron microscopy. Results: α-synuclein overexpression in the cells resulted in the alteration of mitochondrial ultrastructure accompanied by the increment of lysosomes number and the accumulation of autophagic-vesicular structures. Conclusion:Overexpression of α-synuclein can lead to autophagy in SH-SY5Y cells in vitro.
作者 张宇新 张子明 杨慧 蔡青 鲁强 陈彪 徐群渊
机构地区 华北煤炭医学院基础医学部 首都医科大学北京神经科学研究所
出处 《解剖学杂志》 CAS CSCD 北大核心 2005年第3期258-260,共3页 Chinese Journal of Anatomy
基金 国家重点基础研究规划("973"计划)课题(G1999054008,G2000057005) 国家自然科学基金(30240055) 北京市自然科学基金(70022005) 河北省自然科学基金(C2004000689)
关键词 Α-SYNUCLEIN 过表达 SH-SY5Y细胞 体外研究 自体吞噬 α-synuclein overexpression SH-SY5Y cells in vitro autophagy
分类号 R329.2 [医药卫生—人体解剖和组织胚胎学]
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参考文献13

  • 1Goedert M. α-synuclein and neurodegenerative diseases. Nat Rev Neurosci, 2001,2(7):492-501.
  • 2Masliah E, Rockenstein E, Veinbergs I, et al. Dopaminergic loss and inclusion body formation in α-synuclein mice: implications for neurodegenerative disorders. Science, 2000,287(5456):1265-1269.
  • 3Feany MB, Bender WW. A drosophila model of Parkinsons disease. Nature, 2000,404(6776):394-398.
  • 4张宇新,杨慧,蔡青,珠帕尔,鲁强,苏月,赵春礼,徐群渊.α-synuclein-EGFP在体外培养SH-SY5Y细胞中过表达对包涵体形成及线粒体结构改变的影响[J].神经解剖学杂志,2003,19(3):251-256. 被引量：7
  • 5Junn E, Mouradian MM. Human α-synuclein over-expression increases intracellular reactive oxygen species levels and susceptibility to dopamine. Neurosci Lett, 2002,320(3):146-150.
  • 6Hsu LJ, Sagara Y, Arroyo A, et al. Alpha-synuclein promotes mitochondrial deficit and oxidative stress. Am J Pathol, 2000,157(2):401-410.
  • 7Lemasters JJ, Nieminen AL, Qian T, et al. The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagey. Biochim Biophys Acta, 1998,1366(1-2):177-196.
  • 8Rodriguez-Enriquez S, He L, Lemasters JJ. Role of mitochondrial permeability transition pores in mitochondrial autophagy. Int J Biochem Cell Biol, 2004,36(12):2463-2472.
  • 9Klionsky DJ, Emr SD. Autophagy as a regulated pathway of cellular degradation. Science, 2000,290(5497):1717-1721.
  • 10Ravikumar B, Duden R, Rubinsztein DC. Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy. Hum Mol Genet, 2002,11(9):1107-1117.

二级参考文献1

  • 1Spector DL et al 黄培堂 等译.Cells A Leboratory Manual(细胞实验指南)[M].北京:科学出版社,2001.986～987.

共引文献6

同被引文献21

  • 1张宇新,张子明,杨慧,蔡青,鲁强,陈彪,徐群渊.α-突触核蛋白在体外培养SH-SY5Y细胞内过表达可导致氧应激[J].中国病理生理杂志,2005,21(8):1532-1535. 被引量：5
  • 2Jenner P.Parkinson’s disease,pesticides and mitochondrial dopamine turnover following acute administration of rotenone to dysfunction. Trends in Neurosciences . 2001
  • 3Dauer W,Przedborski S.Parkinson’s disease: mechanisms and models. Neuron . 2003
  • 4Conway K A,Lee S J,Rochet J C,et al.Acceleration of oligomerization, not fibrillization, is a shared property of both alpha-synuclein mutations linked to early-onset Parkinson’s disease: implications for pathogenesis and therapy. Proceedings of the National Academy of Sciences of the United States of America . 2000
  • 5Di Monte DA.The environment and Parkinson’s disease: is the nigrostriatal system preferentially targeted by neurotoxins?. Lancet Neurology,The . 2003
  • 6Thiffault C,Langston J W,Di Monte D A.Increased striatal dopamine turnover following acute administration of rotenone to mice. Brain Research . 2000
  • 7Trounce I A,Kim Y L,Jun A S,et al.Assessment of mitochondrial oxidative phosphorylation in patient muscle biopsies, lymphoblasts, and transmitochondrial cell lines. Methods in Enzymology . 1996
  • 8Turrens JF,Boveris A.Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria. Biochemical Journal . 1980
  • 9Hsu LJ,Sagara Y,Arroyo A,et al.Alpha-synuclein promotes mitochondrial deficit and oxidative stress. American Journal of Pathology . 2000
  • 10von Bohlen und Halbach O,Schober A,Krieglstein K.Genes, proteins, and neurotoxins involved in Parkinson’s disease. Progress in Neurobiology . 2004

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二级引证文献3

解剖学杂志
2005年 第3期

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