کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341310 | 1295830 | 2007 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Thiamine deficiency induces endoplasmic reticulum stress in neurons
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کلمات کلیدی
SmTNUPRCGNseIF2αDAPIGRPATFIREGADD153DcfCM-H2DCFDA2,7-dichlorofluoresceinPBSTPBSWernicke-Korsakoff syndromewks3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromide4,6-diamidino-2-phenylindole - 4،6-دیامیدین-2-فنیلینولMTT - MTTROS - ROSAlzheimer’s disease - بیماری آلزایمرParkinson’s disease - بیماری پارکینسونNutrition - تغذیهNeurodegeneration - تولید نوروژنیکendoplasmic reticulum - شبکه آندوپلاسمی phosphate buffer saline - فسفات بافر شورactivating transcription factor - فعال کردن عامل رونویسیCerebellum - مخچهCell death - مرگ سلولی cerebellar granule neurons - نورونهای گرانشی مخچهVitamin B1 - ویتامین B1Unfolded protein response - پاسخ پروتئین آشکارglucose-regulated protein - پروتئین تنظیم شده با گلوکزPERK - پرکthiamine deficiency - کمبود تیامینReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Thiamine deficiency induces endoplasmic reticulum stress in neurons Thiamine deficiency induces endoplasmic reticulum stress in neurons](/preview/png/4341310.png)
چکیده انگلیسی
Thiamine (vitamin B1) deficiency (TD) causes region selective neuronal loss in the brain; it has been used to model neurodegeneration that accompanies mild impairment of oxidative metabolism. The mechanisms for TD-induced neurodegeneration remain incompletely elucidated. Inhibition of protein glycosylation, perturbation of calcium homeostasis and reduction of disulfide bonds provoke the accumulation of unfolded proteins in the endoplasmic reticulum (ER), and cause ER stress. Recently, ER stress has been implicated in a number of neurodegenerative models. We demonstrated here that TD up-regulated several markers of ER stress, such as glucose-regulated protein (GRP) 78, growth arrest and DNA-damage inducible protein or C/EBP-homologus protein (GADD153/Chop), phosphorylation of eIF2α and cleavage of caspase-12 in the cerebellum and the thalamus of mice. Furthermore, ultrastructural analysis by electron microscopic study revealed an abnormality in ER structure. To establish an in vitro model of TD in neurons, we treated cultured cerebellar granule neurons (CGNs) with amprolium, a potent inhibitor of thiamine transport. Exposure to amprolium caused apoptosis and the generation of reactive oxygen species in CGNs. Similar to the observation in vivo, TD up-regulated markers for ER stress. Treatment of a selective inhibitor of caspase-12 significantly alleviated amprolium-induced death of CGNs. Thus, ER stress may play a role in TD-induced brain damage.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 144, Issue 3, 9 February 2007, Pages 1045-1056
Journal: Neuroscience - Volume 144, Issue 3, 9 February 2007, Pages 1045-1056
نویسندگان
X. Wang, B. Wang, Z. Fan, X. Shi, Z.-J. Ke, J. Luo,