Articles

Effects of α-Synuclein Protein Overexpression on Mice Striatum

  • DUAN Jinyan ,
  • LIU Kefu ,
  • ZHANG Yongqian ,
  • ZHANG Yanyan ,
  • QING Hong ,
  • DENG Yulin
Expand
  • School of Life Science, Beijing Institute of Technology, Beijing 100081, China

Received date: 2013-08-26

  Revised date: 2013-12-09

  Online published: 2014-03-26

Abstract

Parkinson's disease (PD) is a common progressive neurodegenerative syndrome. The α- synuclein(α- syn)is a major protein constituent of Lewy bodies, and the α-syn A30P mutant causes familial autosomal dominant PD. In the present study, we explored the effect of α-syn overexpression and its mutant α-syn A30P on mice striatum. The behavior of PDGF-h α-synucleinWT and PDGF-h α-synucleinA30P transgenic mice was investigated, and the oxidative stress levels and the concentration of catecholamine isoquinolines (CAIQs) were determined in transgenic mice striatum, respectively. Compared to the control group, the coordination abilities of the two types of transgenic mice decreased. In addition, the level of oxidative stress and the concentration of CAIQs significantly increased in the overexpression of α-syn WT and α-syn A30P mice striatum. Thus, it is concluded that overexpression of α-syn and its mutant α-syn A30P exhibit impairment in the striatum through increasing the level of oxidative stress and CAIQs.

Cite this article

DUAN Jinyan , LIU Kefu , ZHANG Yongqian , ZHANG Yanyan , QING Hong , DENG Yulin . Effects of α-Synuclein Protein Overexpression on Mice Striatum[J]. Science & Technology Review, 2014 , 32(7) : 22 -26 . DOI: 10.3981/j.issn.1000-7857.2014.07.002

References

[1] Thomas B, Beal M F. Parkinson's disease[J]. Human Molecular Genetics, 2007, 16(R2): R183-R194.
[2] De Rijk M C, Launer L J, Berger K, et al. Prevalence of Parkinson's disease in Europe: A collaborative study of population-based cohorts. Neurologic diseases in the elderly research group[J]. Neurology, 2000, 54(11 S5): 21-23.
[3] Polymeropoulos M H, Higgins J J, Golbe L I, et al. Mapping of a gene for Parkinson's disease to chromosome 4q21-q23[J]. Science, 1996, 274 (5290): 1197-1199.
[4] Kruger R,KuhnW,MullerT,etal.Ala30Promutationinthegeneencoding α- synuclein in Parkinson's disease[J]. Nature Genetics, 1998, 18(2): 106-108.
[5] Zarranz J J, Alegre J, Gomez-Esteban J C, et al. The new mutation, E46K, of α-synuclein causes Parkinson and Lewy body dementia[J]. Annals of Neurology, 2004, 55(2): 164-173.
[6] Garcia-Reitbock P, Anichtchik O, Dalley J W, et al. Endogenous α- synuclein influences the number of dopaminergic neurons in mouse substantia nigra[J]. Experimental Neurology, 2013, 248: 541-545.
[7] George S, Rey N L, Reichenbach N, et al. α-Synuclein: the long distance runner[J]. Brain Pathology, 2013, 23(3): 350-357.
[8] Bendor J T, Logan T P, Edwards R H. The Function of α-Synuclein[J]. Neuron, 2013, 79(6): 1044-1066.
[9] Lotharius J, Brundin P. Pathogenesis of Parkinson's disease: Dopamine, vesicles and α-synuclein[J]. Nature Reviews Neuroscience, 2002, 3(12): 932-942.
[10] Lane E, Dunnett S. Animal models of Parkinson's disease and L-dopa induced dyskinesia: How close are we to the clinic?[J]. Psychopharma- cology, 2008, 199(3): 303-312.
[11] Blesa J, Phani S, Jackson-Lewis V, et al. Classic and new animal models of Parkinson's disease[J/OL]. Journal of Biomedicine & Bio- technology,2012,[2013-12-09]. http://dx.doi.org/10.1155/2012/845618.
[12] Krüger R, Kuhn W, Müller T, et al. AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease[J]. Nature Genetics, 1998, 18(2): 106-108.
[13] Chinta S J, Lieu C A, Demaria M, et al. Environmental stress, ageing and glial cell senescence: A novel mechanistic link to Parkinson's disease?[J]. Journal of Internal Medicine, 2013, 273(5): 429-436.
[14] Singleton A B, Farrer M J, Bonifati V. The genetics of Parkinson's disease: Progress and therapeutic implications[J]. Movement Disorders, 2013, 28(1): 14-23.
[15] Kang J H. Salsolinol, a catechol neurotoxin, induces oxidative modifi- cation of cytochrome c[J]. BMB Reports, 2013, 46(2): 119-123.
[16] Su Y, Duan J, Ying Z, et al. Increased vulnerability of parkin knock down PC12 cells to hydrogen peroxide toxicity: The role of salsolinol and NM-salsolinol[J]. Neuroscience, 2013, 233: 72-85.
[17] Witt S N, Flower T R. α-Synuclein, oxidative stress and apoptosis from the perspective of a yeast model of Parkinson's disease[J]. FEMS Yeast Research, 2006, 6(8): 1107-1116.
Outlines

/