کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10765319 | 1050592 | 2010 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dopamine facilitates α-synuclein oligomerization in human neuroblastoma SH-SY5Y cells
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Parkinson's disease is characterized by selective loss of dopaminergic neurons in the substantia nigra and by the appearance of Lewy bodies. Fibrillar α-synuclein is the main component of Lewy bodies. Previous studies have suggested that dopamine promotes α-synuclein oligomerization and that partially aggregated or oligomeric α-synuclein could be cytotoxic. To confirm this hypothesis using cell cultures, we performed size exclusion chromatography as a pretreatment method prior to Western blotting to more clearly detect a small amount of α-synuclein oligomers in wild-type α-synuclein-overexpressing SH-SY5Y cells. Using this method, we confirmed that stable overexpression of α-synuclein in SH-SY5Y cells indeed increased the amounts of α-synuclein oligomers in these cells and exposure of the cells to dopamine for 6 h facilitated α-synuclein oligomerization. These dopamine-induced α-synuclein oligomers continued to exist for the following 24 h. However, the dopamine-treated cells did not undergo cell death or apoptosis in spite of the presence of increased oligomeric α-synuclein. Our data may contribute to the understanding of the mechanisms underlying α-synuclein oligomer formation and its suspected cytotoxicity toward dopaminergic neurons.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 391, Issue 1, 1 January 2010, Pages 129-134
Journal: Biochemical and Biophysical Research Communications - Volume 391, Issue 1, 1 January 2010, Pages 129-134
نویسندگان
Kentaro Yamakawa, Yasuhiko Izumi, Hiroki Takeuchi, Noriyuki Yamamoto, Toshiaki Kume, Akinori Akaike, Ryosuke Takahashi, Shun Shimohama, Hideyuki Sawada,