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STI571 protects neuronal cells from neurotoxic prion protein fragment-induced apoptosis

Pan, Yaoqian, Sun, Liyong, Wang, Jihong, Fu, Wenzhuo, Fu, Yongyao, Wang, Jin, Tong, Yigang, Pan, Bo·2015·Neuropharmacology
DOI 10.1016/j.neuropharm.2015.01.029
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Abstract

Prion diseases are neurodegenerative disorders caused by the accumulation of misfolded prion proteins [scrapie form of PrP (PrP(Sc))]. PrP(Sc) accumulation in the brain causes neurotoxicity by inducing mitochondrial-apoptotic pathways. Neurodegeneration can be prevented by imatinib mesylate (Gleevec or STI571) that regulates c-Abl tyrosine kinases, which elicit protective effects in neurodegenerative disease models. However, the protective effect of STI571 against prion disease remains unknown. In the present study, the effect of STI571 on prion peptide-induced neuronal death was investigated. Results showed that STI571 rescued neurons from PrP106-126-induced neurotoxicity by preventing mitochondrial dysfunction. STI571-inhibited c-Abl tyrosine kinases prevented PrP106-126-induced reduction in mitochondrial potential, Bax translocation to the mitochondria and cytochrome c release. The protective effect of STI571 against mitochondrial dysfunction was related to the activation of BIM expression. This study is the first to demonstrate the protective effect of STI571 against prion-mediated neurotoxicity. Our results suggested that imatinib mesylate treatment may be a novel therapeutic strategy to treat prion-mediated neurotoxicity.

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Metadata

Authors
Pan, Y., Sun, L., Wang, J., Fu, W., Fu, Y., Wang, J., Tong, Y., & Pan, B.
ORCID
Pan, Yaoqian
Venue
Neuropharmacology
Publisher
Elsevier BV
Published
2015-06
Volume
93
Pages
191-198
ISSN
0028-3908
DOI
10.1016/j.neuropharm.2015.01.029
Cited by
33
References
3
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
  • National Natural Science Foundation of China (31372407)
  • Henan Scientific and technological project (132102110118)

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