کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9001600 | 1118537 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Evaluation of the neuronal apoptotic pathways involved in cytoskeletal disruption-induced apoptosis
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کلمات کلیدی
Serine-proteasesdpqAc-DEVD-choTLCKPVDFz-FA-FMKPARPFCSCGNsMTT - MTTNα-p-tosyl-l-lysine chloromethyl ketone - N-p-tosyl-l-lysine chloromethyl ketoneAIF - آیفونBAPTA-AM - بیایپیتیای-AMfoetal calf serum - سرم گوساله جنینapoptosis inducing factor - عامل القاء آپوپتوزcerebellar granule neurons - نورونهای گرانشی مخچهPropidium iodide - پروتئین یدیدPolyvinylidene fluoride - پلی وینیلیدین فلورایدCytoskeleton - چارچوب یاخته، سیتواسکلتون، اسکلت سلولیCaspases - کاسپازCalcium - کلسیم
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The cytoskeleton is critical to neuronal functioning and survival. Cytoskeletal alterations are involved in several neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. We studied the possible pathways involved in colchicine-induced apoptosis in cerebellar granule neurons (CGNs). Although colchicine evoked an increase in caspase-3, caspase-6 and caspase-9 activation, selective caspase inhibitors did not attenuate apoptosis. Inhibitors of other cysteine proteases such as PD150606 (a calpain-specific inhibitor), Z-Phe-Ala fluoromethyl ketone (a cathepsins-inhibitors) and Nα-p-tosyl-l-lysine chloromethyl ketone (serine-proteases inhibitor) also had no effect on cell death/apoptosis induced by colchicine. However, BAPTA-AM 10 μM (intracellular calcium chelator) prevented apoptosis mediated by cytoskeletal alteration. These data indicate that calcium modulates colchicine-induced apoptosis in CGNs. PARP-1 inhibitors did not prevent apoptosis mediated by colchicine. Finally, colchicine-induced apoptosis in CGNs was attenuated by kenpaullone, a cdk5 inhibitor. Kenpaullone and indirubin also prevented cdk5/p25 activation mediated by colchicine. These findings indicate that cytoskeletal alteration can compromise cdk5 activation, regulating p25 formation and suggest that cdk5 inhibitors attenuate apoptosis mediated by cytoskeletal alteration. The present data indicate the potential therapeutic value of drugs that prevent the formation of p25 for the treatment of neurodegenerative disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 70, Issue 3, 1 August 2005, Pages 470-480
Journal: Biochemical Pharmacology - Volume 70, Issue 3, 1 August 2005, Pages 470-480
نویسندگان
Elvira G. Jordà , Ester Verdaguer, Andrés Jimenez, S. Garcia de Arriba, Clemens Allgaier, Mercè Pallà s, Antoni Camins,