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Analysis of heat-shock protein 70 gene polymorphisms and the risk of Parkinson’s disease

Content Provider	Springer Nature Link
Author	Wu, Yih Ru Wang, Cheng Kuang Chen, Chiung Mei Hsu, Yuying Lin, Sih Jing Lin, Yi Ying Fung, Hon Chung Chang, Kuo Hsuan Lee Chen, Guey Jen
Copyright Year	2004
Abstract	Parkinson’s disease (PD) involves several genetic and environmental components. Heat-shock protein 70, a chaperone that is up-regulated in stress responses and that refolds protein, may be involved in the pathogenesis of PD. We have investigated the association of polymorphisms −110 A/C, +190 G/C, +1267 A/G, +2074 G/C, and +2437 G/C in the 5’ and coding regions of the HSP70-1, HSP70-2, and HSP70-hom genes with the risk of PD by screening DNA samples from 274 PD patients and 183 controls in assays based on the polymerase chain reaction. There was no statistically significant difference in genotype distribution between patients and controls for the three coding-region polymorphisms in HSP70-2 and HSP70-hom. However, for HSP70-1, the overall genotype distribution was significantly different at the −110 site (P=0.004) and tended to be different at the +190 site (P=0.012) between patients and controls. The frequencies of the −110 CC and +190 CC genotypes were significantly higher in PD patients than in controls (P=0.001 and 0.006, respectively). Both −110 CC (odds ratio: 2.91; 95% CI: 1.51–5.96; P=0.002) and +190 CC (odds ratio: 3.59; 95% CI: 1.53–9.88; P=0.006) genotypes were significantly associated with PD. Reporter constructs containing the −110 A allele cloned into a luciferase reporter plasmid drove marginally higher transcriptional activity of HSP70-1 compared with the −110 C allele in both control and heat-shocked IMR32 and 293 cells. Therefore, −110 A/C may be a functional polymorphism in the 5’ promoter region of HSP70-1 and may affect susceptibility to PD.
Starting Page	236
Ending Page	241
Page Count	6
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	114
Issue Number	3
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	2003-11-06
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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