Proteome analysis of human substantia nigra in Parkinson's disease

被引：209
作者：
Basso, M
Giraudo, S
Corpillo, D
Bergamasco, B
Lopiano, L
Fasano, M
机构：
[1] Univ Insubria, Ctr Neurosci, Arsizio, VA, Italy
[2] Univ Insubria, Dept Struct & Funct Biol, Arsizio, VA, Italy
[3] Univ Turin, Dept Neurosci, Turin, Italy
[4] Bioind Pk Canavese, Colleretto Giacosa, Italy
[5] Salvatore Maugeri Fdn, Pavia, Italy
来源：
PROTEOMICS | 2004年 / 4卷 / 12期
关键词：
excitotoxicity; mitochondrial impairment; oxidative stress; Parkinson's disease; protein expression;
D O I：
10.1002/pmic.200400848
中图分类号：
Q5 [生物化学];
学科分类号：
071010 ; 081704 ;
摘要：
Protein expression has been compared in human substantia nigra specimens from Parkinson's disease (PD) patients and from controls, and 44 proteins expressed in this midbrain region were identified by peptide mass fingerprinting. Among them, nine showed changes in their abundance. L and M neurofilament chains are less abundant in PD specimens, whereas peroxiredoxin II, mitochondrial complex III, ATP synthase D chain, complexin I, profilin, L-type calcium channel delta-subunit, and fatty-acid binding protein are significantly more present in PD samples than in controls. Besides the consolidated view of oxidative stress involvement in PD pathogenesis, suggested by overexpression of mitochondrial and reactive oxygen species (ROS)-scavenging proteins, these results indicate a possible potentiation mechanism of afferent signals to substantia nigra following degeneration of dopaminergic neurons.
引用
收藏
页码：3943 / 3952
页数：10
相关论文
共 50 条
[41]  
Przedborski S, 2000, OXIDAT STRESS DIS, P273
[42]  
Schonberger SJ, 2001, PROTEOMICS, V1, P1519, DOI 10.1002/1615-9861(200111)1:12<1519::AID-PROT1519>3.0.CO
[43]  
2-L
[44]   Molecular pathogenesis of movement disorders: are protein aggregates a common link in neuronal degeneration? [J].
Schulz, JB ;
Dichgans, J .
CURRENT OPINION IN NEUROLOGY, 1999, 12 (04) :433-439
[45]  
Sinha P, 2001, PROTEOMICS, V1, P835, DOI 10.1002/1615-9861(200107)1:7<835::AID-PROT835>3.0.CO
[46]  
2-2
[47]   alpha-synuclein in Lewy bodies [J].
Spillantini, MG ;
Schmidt, ML ;
Lee, VMY ;
Trojanowski, JQ ;
Jakes, R ;
Goedert, M .
NATURE, 1997, 388 (6645) :839-840
[48]   Expression of mutant α-synuclein causes increased susceptibility to dopamine toxicity [J].
Tabrizi, SJ ;
Orth, M ;
Wilkinson, JM ;
Taanman, JW ;
Warner, TT ;
Cooper, JM ;
Schapira, AHV .
HUMAN MOLECULAR GENETICS, 2000, 9 (18) :2683-2689
[49]   Inducible expression of mutant α-synuclein decreases proteasome activity and increases sensitivity to mitochondria-dependent apoptosis [J].
Tanaka, Y ;
Engelender, S ;
Igarashi, S ;
Rao, RK ;
Wanner, T ;
Tanzi, RE ;
Sawa, A ;
Dawson, VL ;
Dawson, TM ;
Ross, CA .
HUMAN MOLECULAR GENETICS, 2001, 10 (09) :919-926
[50]   α-synuclein fibrillogenesis is nucleation-dependent -: Implications for the pathogenesis of Parkinson's disease [J].
Wood, SJ ;
Wypych, J ;
Steavenson, S ;
Louis, JC ;
Citron, M ;
Biere, AL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (28) :19509-19512
12345