Identification of genes associated with paraquat-induced toxicity in SH-SY5Y cells by PCR array focused on apoptotic pathways

被引:28
作者
Moran, Jose M. [1 ]
Gonzalez-Polo, Rosa A. [1 ]
Ortiz-Ortiz, Miguel A. [1 ]
Niso-Santano, Mireia [1 ]
Soler, German [1 ]
Fuentes, Jose M. [1 ]
机构
[1] Univ Extremadura, Dept Bioquim Biol Mol & Genet, EU Enfermeria & TO, EU Enfermeria & TO, Caceres 10071, Spain
来源
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES | 2008年 / 71卷 / 22期
关键词
D O I
10.1080/15287390802329364
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Paraquat (PQ) (1,1-dimethyl-4,4'-bipyridinium dichloride), a widely used herbicide, has been suggested as a potential etiologic factor for the development of Parkinson's disease (PD). In this sense, understanding of the molecular mechanism underlying PQ-induced toxicity to neural cells is important for optimal use as well as for the development of new drugs. To gain insights into PQ-induced neurotoxicity, polymerase chain reaction (PCR) array analysis focused on a panel of apoptosis-related genes was performed using neuroblastoma SH-SY5Y cells. Up to 65 apoptosis-related genes were monitored. Our analysis of apoptotic process through microarray technology showed that in PQ-induced neuroblastoma SH-SY5Y cells, there is a different expression of BIK, CASP3, CASP7, CRADD, DAPK, FAS, and other related genes, in comparison to unstimulated cells. Evaluation of genes regulated differentially is essential for the development of therapeutic approaches in multifactorial diseases as PD. Our data provide a useful basis for screening candidate targets for early diagnosis and further intervention in PQ-mediated toxicity of neural cells. Paraquat (PQ) (1,1-dimethyl-4,4'-bipyridinium dichloride), a widely used herbicide, has been suggested as a potential etiologic factor for the development of Parkinson's disease (PD). In this sense, understanding of the molecular mechanism underlying PQ-induced toxicity to neural cells is important for optimal use as well as for the development of new drugs. To gain insights into PQ-induced neurotoxicity, polymerase chain reaction (PCR) array analysis focused on a panel of apoptosis-related genes was performed using neuroblastoma SH-SY5Y cells. Up to 65 apoptosis-related genes were monitored. Our analysis of apoptotic process through microarray technology showed that in PQ-induced neuroblastoma SH-SY5Y cells, there is a different expression of BIK, CASP3, CASP7, CRADD, DAPK, FAS, and other related genes, in comparison to unstimulated cells. Evaluation of genes regulated differentially is essential for the development of therapeutic approaches in multifactorial diseases as PD. Our data provide a useful basis for screening candidate targets for early diagnosis and further intervention in PQ-mediated toxicity of neural cells.
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收藏
页码:1457 / 1467
页数:11
相关论文
共 59 条
[11]   Dopaminergic cell death induced by MPP+, oxidant and specific neurotoxicants shares the common molecular mechanism [J].
Chun, HS ;
Gibson, GE ;
DeGiorgio, LA ;
Zhang, H ;
Kidd, VJ ;
Son, JH .
JOURNAL OF NEUROCHEMISTRY, 2001, 76 (04) :1010-1021
[12]   Hypoxia, BNip3 proteins, and the mitochondrial death pathway in cardiomyocytes [J].
Crow, MT .
CIRCULATION RESEARCH, 2002, 91 (03) :183-185
[13]   Neuronal apoptosis-inhibitory protein does not interact with Smac and requires ATP to bind caspase-9 [J].
Davoodi, J ;
Lin, L ;
Kelly, J ;
Liston, P ;
MacKenzie, AE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (39) :40622-40628
[14]   Deficiency of inducible nitric oxide synthase protects against MPTP toxicity in vivo [J].
Dehmer, T ;
Lindenau, J ;
Haid, S ;
Dichgans, J ;
Schulz, JB .
JOURNAL OF NEUROCHEMISTRY, 2000, 74 (05) :2213-2216
[15]  
Di Monte DA, 2000, MOVEMENT DISORD, V15, P459, DOI 10.1002/1531-8257(200005)15:3<459::AID-MDS1006>3.0.CO
[16]  
2-3
[17]   Peptide inhibitors of caspase-3-like proteases attenuate 1-methyl-4-phenylpyridinum-induced toxicity of cultured fetal rat mesencephalic dopamine neurons [J].
Dodel, RC ;
Du, Y ;
Bales, KR ;
Ling, ZD ;
Carvey, PM ;
Paul, SM .
NEUROSCIENCE, 1998, 86 (03) :701-707
[18]   Gene expression profiling of aging reveals activation of a p53-mediated transcriptional program [J].
Edwards, Michael G. ;
Anderson, Rozalyn M. ;
Yuan, Ming ;
Kendziorski, Christina M. ;
Weindruch, Richard ;
Prolla, Tomas A. .
BMC GENOMICS, 2007, 8
[19]   Fas and Fas-L expression in Huntington's disease and Parkinson's disease [J].
Ferrer, I ;
Blanco, R ;
Cutillas, B ;
Ambrosio, S .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2000, 26 (05) :424-433
[20]  
Gómez C, 2001, J NEUROSCI RES, V63, P421, DOI 10.1002/1097-4547(20010301)63:5<421::AID-JNR1037>3.0.CO