کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10958394 | 1100047 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CD40-CD40L interactions promote neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism
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کلمات کلیدی
EAESmTNpotassium phosphate buffered salineTNFINF-γCD40LKPBSCD40NeuNDABGFAPICAM-13,3′-diaminobenzidine - 3،3'-diaminobenzidineBSA - BSAbovine serum albumin - آلبومین سرم گاوexperimental autoimmune encephalomyelitis - آنسفالومیلیت خودایمنی تجربیinterferon-gamma - اینترفرون گاماAlzheimer's disease - بیماری آلزایمرParkinson's disease - بیماری پارکینسونNeurodegeneration - تولید نوروژنیکThiamine - تیامین، ویتامین B1CNS - دستگاه عصبی مرکزیcentral nervous system - سیستم عصبی مرکزیtumor necrosis factor - فاکتور نکروز تومورCD40 ligand - لیگاند CD40Oxidative metabolism - متابولیسم اکسیداتیوintercellular adhesion molecule-1 - مولکول چسبندگی بین سلولی -1Microglia - میکروگلیاهاGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالneuronal specific nuclear protein - پروتئین هسته ای خاص نورونیthiamine deficiency - کمبود تیامین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: CD40-CD40L interactions promote neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism CD40-CD40L interactions promote neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism](/preview/png/10958394.png)
چکیده انگلیسی
Abnormalities in oxidative processes, region-selective neuron loss, inflammation and diminished activity of thiamine-dependent enzymes characterize age-related neurodegenerative diseases. Thiamine deficiency (TD) models the selective neurodegeneration that accompanies mild impairment of oxidative metabolism. As in human neurodegenerative diseases, alterations in multiple cell types accompany the TD-induced neurodegeneration. The current studies demonstrate that CD40 and CD40 ligand (CD40L), two co-stimulatory immune molecules, are involved in TD-induced selective neuronal death. TD induced CD40 immunoreactivity in microglia and CD40L immunoreactivity in astrocytes. Both CD40-positive microglia and CD40L-positive astrocytes increased during the progressive TD-induced neuronal death. In early stages of TD, targeted deletion of CD40 diminished the number of CD40L-positive astrocytes and reduced neuronal death by 35%. The number of CD40L-positive astrocytes increased whenever the number of NeuN-positive neurons decreased. In early stages of TD, deletion of CD40L diminished CD40-positive microglia and reduced the neuronal death by 64%. In advanced phases of TD, neither CD40 nor CD40L deletion protected against neuronal death. The data show for the first time that TD induces expression of CD40 by the microglia and CD40L by astrocytes. The results indicate that CD40-CD40L interactions promote neuronal death in early stages of TD, but that at later phases the protective effects of the diminished CD40 or CD40L are over-ridden by other mechanisms.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 47, Issue 3, August 2005, Pages 204-215
Journal: Neurochemistry International - Volume 47, Issue 3, August 2005, Pages 204-215
نویسندگان
Zun-Ji Ke, Noel Y. Calingasan, Lorraine A. DeGiorgio, Bruce T. Volpe, Gary E. Gibson,