Abstract：
:The prion diseases are neurodegenerative disorders characterized by the conversion of the PrPc (normal cellular prion) to the PrPsc (misfolded isoform). The accumulation of PrPsc within the central nervous system (CNS) leads to neurocytotoxicity by increasing oxidative stress. In addition, many neurodegenerative disorders including prion, Parkinson's and Alzheimer's diseases may be regulated by cholesterol homeostasis. The effects of cholesterol balance on prion protein-mediated neurotoxicity and ROS (reactive oxygen species) generation were the focus of this study. Cholesterol treatment inhibited PrP (106-126)-induced neuronal cell death and ROS generation in SH-SY5Y neuroblastoma cells. In addition, the PrP (106-126)-mediated increase of p53, p-p38, p-ERK and the decrease of Bcl-2 were blocked by cholesterol treatment. These results indicated that cellular cholesterol enrichment is a key regulator of PrP-106-126-mediated oxidative stress and neurotoxicity. Taken together, the results of this study suggest that modulation of cellular cholesterol appears to prevent the neuronal cell death caused by prion peptides.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Jeong JK,Seol JW,Moon MH,Seo JS,Lee YJ,Kim JS,Park SYdoi
10.1016/j.bbrc.2010.09.078subject
Has Abstractpub_date
2010-10-29 00:00:00pages
516-20issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(10)01775-4journal_volume
401pub_type
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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更新日期：2016-09-09 00:00:00
