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PEP‐1‐heat shock protein 27 protects from neuronal damage in cells and in a Parkinson’s disease mouse model
Author(s) -
Lee Yeom Pyo,
Kim Dae Won,
Kang Hye Won,
Hwang Jae Hyeok,
Jeong Hoon Jae,
Sohn Eun Jeong,
Kim Mi Jin,
Ahn Eun Hee,
Shin Min Jea,
Kim DukSoo,
Kang TaeCheon,
Kwon OhShin,
Cho SungWoo,
Park Jinseu,
Eum Won Sik,
Choi Soo Young
Publication year - 2012
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2012.08574.x
Subject(s) - hsp27 , substantia nigra , oxidative stress , mptp , heat shock protein , reactive oxygen species , parkinson's disease , microbiology and biotechnology , dopaminergic , biology , chemistry , hsp70 , neuroscience , biochemistry , dopamine , medicine , disease , gene
Heat shock proteins (HSPs) are a highly conserved family of proteins that are induced in response to various environmental stressors including reactive oxygen species. HSP27 is a chaperone protein with the ability to increase cell survival in response to oxidative stress. Parkinson’s disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons. Although the mechanism of PD remains unclear, oxidative stress is known to be important in its pathogenesis. This study investigated the protective effects of PEP‐1‐HSP27 on neuronal damage induced by 1‐methyl‐4‐phenyl pyridinium (MPP + ) in SH‐SY5Y cells and in a 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced PD mouse model. PEP‐1‐HSP27 rapidly entered the cells and protected them against MPP + ‐induced toxicity by inhibiting the reactive oxygen species levels and DNA fragmentation. Furthermore, transduced PEP‐1‐HSP27 prevented dopaminergic neuronal cell death in the substantia nigra of MPTP‐induced PD mouse models. These results demonstrate that PEP‐1‐HSP27 provides a potential strategy for therapeutic delivery against various diseases and is a potential tool for the treatment of PD.