کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4343618 | 1615119 | 2014 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Methylglyoxal reduces mitochondrial potential and activates Bax and caspase-3 in neurons: Implications for Alzheimer's disease
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
d-glyceraldehyde-3-phosphateFBSTriose-phosphate isomerasenNOSTriosephosphate isomeraseAβDHAPAGEsTPI3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromide3-nitrotyrosine - 3-نیتروتیروستینMTT - MTTamyloid β-peptide - β-پپتید آمیلوئیدHydrogen peroxide - آب اکسیژنهAmyloid - آمیلوئیدoverexpressing - بیش از حد بیانAlzheimer disease - بیماری آلزایمرApoptosis - خزان یاختهایdihydroxyacetone phosphate - دی هیدروکسی استون فسفاتfetal bovine serum - سرم جنین گاوGAP - شکافMethylglyoxal - متیل گلی اکسالadvanced glycation end-products - محصولات نهایی گلیسایی پیشرفتهwild type - نوع وحشیNeuronal NO synthase - نیاسین سنتاز NONitric oxide - نیتریک اکسیدH2O2 - هیدروژن پراکسیدAntibody - پادتَن یا آنتیبادی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Alzheimer's disease (AD) is characterized by the oxidative stress generated from amyloid β-peptide (Aβ) aggregates. It produces protein nitrotyrosination, after the reaction with nitric oxide to form peroxynitrite, being triosephosphate isomerase (TPI) one of the most affected proteins. TPI is a glycolytic enzyme that catalyzes the interconversion between glyceraldehyde 3-phosphate (GAP) and dihydroxyacetone phosphate (DHAP). Methylglyoxal (MG) is a by-product of TPI activity whose production is triggered when TPI is nitrotyrosinated. MG is harmful to cells because it glycates proteins. Here we found protein glycation when human neuroblastoma cells were treated with Aβ. Moreover glycation was also observed when neuroblastoma cells overexpressed mutated TPI where Tyr165 or Tyr209, the two tyrosines close to the catalytic center, were changed by Phe in order to mimic the effect of nitrotyrosination. The pathological relevance of these findings was studied by challenging cells with Aβ oligomers and MG. A significant decrease in mitochondrial transmembrane potential, one of the first apoptotic events, was obtained. Therefore, increasing concentrations of MG were assayed searching for MG effect in neuronal apoptosis. We found a decrease of the protective Bcl2 and an increase of the proapoptotic caspase-3 and Bax levels. Our results suggest that MG is triggering apoptosis in neurons and it would play a key role in AD neurodegeneration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 580, 19 September 2014, Pages 78-82
Journal: Neuroscience Letters - Volume 580, 19 September 2014, Pages 78-82
نویسندگان
Marta Tajes, Abel Eraso-Pichot, Fanny Rubio-Moscardó, Biuse Guivernau, Mònica Bosch-Morató, Victòria Valls-Comamala, Francisco J. Muñoz,