کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10757787 | 1050399 | 2013 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A compound CP-31398 suppresses excitotoxicity-induced neurodegeneration
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کلمات کلیدی
p53GFPDAPI4′,6′-diamidino-2-phenylindole - 4 '، 6'-diamidino-2-phenylindoleMitochondrial dysfunction - اختلال در عملکرد میتوکندریamyotrophic lateral sclerosis - اسکلروز جانبی آمیوتروفیکexcitotoxicity - اکسید سمیتAlzheimer’s disease - بیماری آلزایمرALS - بیماری اسکلروز جانبی آمیوتروفیکParkinson’s disease - بیماری پارکینسونNeurodegeneration - تولید نوروژنیکCNS - دستگاه عصبی مرکزیDIV - دیوdays in vitro - روز in vitrocentral nervous system - سیستم عصبی مرکزیgreen fluorescent protein - پروتئین فلورسنت سبزPropidium iodide - پروتئین یدید
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Neurodegeneration causes dysfunction and degeneration of neurons and is triggered by various factors including genetic defects, free radicals, injury, and glutamate excitotoxicity. Among those, glutamate excitotoxicity is implicated in chronic disorders including AD and ALS, and in acute insults in the CNS including traumatic brain injury. Neurological disorders show hallmark morphological abnormalities such as axon degeneration and cell body death. The molecular mechanisms underlying excitotoxicity-induced neurodegeneration are complex and deciphering a molecular mechanism from one angle is beneficial to understand the process, however, still difficult to develop strategies to suppress excitotoxicity-induced degeneration due to existence of other mechanisms. Thus, directly identifying compounds that can modulate excitotoxicity-induced neurodegeneration and subsequently clarifiying the molecular mechanism is a valid approach to develop effective strategies to suppress neurodegeneration. We searched for compounds that can suppress excitotoxicity-induced neurodegeneration and found that CP-31398, a known compound that can rescue the structure and function of the tumor suppressor protein p53 mutant form and stabilize the active conformation of the p53 wild-type form, suppresses excitotoxicity-induced axon degeneration and cell body death. Moreover, CP-31398 suppresses mitochondrial dysfunction which has a strong correlation with excitotoxicity. Thus, our findings identify a compound that can serve as a novel modulator of neurodegeneration induced by glutamate excitotoxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 440, Issue 3, 25 October 2013, Pages 359-363
Journal: Biochemical and Biophysical Research Communications - Volume 440, Issue 3, 25 October 2013, Pages 359-363
نویسندگان
Takeshi Fujiwara, Koji Morimoto,