Journal
EXPERIMENTAL NEUROLOGY
Volume 176, Issue 1, Pages 262-265Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/exnr.2002.7933
Keywords
3-NP; HSP-70; Huntington's disease; malonate
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Funding
- NCCIH NIH HHS [AT00613] Funding Source: Medline
- NIA NIH HHS [AG12992, AG13846] Funding Source: Medline
- NINDS NIH HHS [NS37102, NS35255, NS 38180] Funding Source: Medline
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Heat shock proteins (HSPs) are induced in response to oxidative stress, hypoxia-ischemia, and neuronal injury and play a protective role. Malonate and 3-nitropropionic acid (3-NP) are well-characterized animal models of Huntington's Disease (HD). They inhibit succinate dehydrogenase, inducing mitochondrial dysfunction, which triggers the generation of superoxide radicals, secondary excitotoxicity, and apoptosis. In this study, we examined whether the 70-kDa heat shock protein (HSP-70) is protective against neurotoxicity induced by malonate and 3-NP. Homozygous and heterozygous HSP-70 overexpressing mice (HSP-70+/+, HSP-70+/-) and wild-type controls received 3-NP or malonate and striatal lesion sizes were evaluated by stereology. Compared to HSP70+/+ and HSP-70+/-, wild-type controls showed significantly larger striatal lesions following 3-NP or malonate injections. These findings support the idea that HSP-70 has a neuroprotective role that may be useful in the treatment of neurodegenerative diseases. (C) 2002 Elsevier Science (USA).
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