کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10958529 | 1100080 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Aβ(31-35) peptide induce apoptosis in PC 12 cells: Contrast with Aβ(25-35) peptide and examination of underlying mechanisms
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
The toxic behaviour of the two shorter sequences of the native Aβ amyloid peptide required for cytotoxicity i.e., Aβ(31-35) and Aβ(25-35) peptides, was studied. We have shown that Aβ(31-35) peptide induces neurotoxicity in undifferentiated PC 12 cell via an apoptotic cell death pathway, including caspase activation and DNA fragmentation. Aβ(25-35) peptide, like the shorter amyloid peptide has the ability to induce neurotoxicity, as evaluated by the MTS reduction assay and by adherent cell count, but the Aβ(25-35) peptide-induced neurotoxicity is not associated with any biochemical features of apoptosis. The differences observed between the neurotoxic properties of Aβ(31-35) and Aβ(25-35) peptides might result on their different ability to be internalised within the neuronal cells. Furthermore, this study reveals that the redox state of methionine residue, C-terminal in Aβ(31-35) and Aβ(25-35) peptides affect in a different way the toxic behaviour of these two short amyloid fragments. Taken together our results suggest that Aβ(31-35) peptide induces cell death by apoptosis, unlike the Aβ(25-35) peptide and that role played by methionine-35 in Aβ induced neurotoxicity might be related to the Aβ aggregation state.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 46, Issue 7, June 2005, Pages 575-583
Journal: Neurochemistry International - Volume 46, Issue 7, June 2005, Pages 575-583
نویسندگان
Francesco Misiti, Beatrice Sampaolese, Michela Pezzotti, Stefano Marini, Massimo Coletta, Lia Ceccarelli, Bruno Giardina, Maria Elisabetta Clementi,