کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10958518 | 1100078 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neurotrophins protect against cytosine arabinoside-induced apoptosis of immature rat cerebellar neurons
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کلمات کلیدی
ERKPKCNT-3NT-4GAPDHPBSBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز DMSO - DMSOPMA - LDC هاMAPK - MAPKMAPK/ERK kinase - MAPK / ERK kinaseMTT - MTTPI 3-kinase - PI 3-کینازTrk - تراکAraC - حق العملDIV - دیوDimethyl sulfoxide - دیمتیل سولفواکسیدdays in vitro - روز in vitrocerebellar granule cells - سلول های گرانول مخچهNeurotoxicity - سمیت عصبیBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزphorbol myristate acetate - فروبل مریستات استاتPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازMEK - مجاهدین خلقNeuroprotection - محافظت نورونی یا محافظت از عصبPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریNeurotrophins - نوروتروفین neurotrophin-3 - نوروتروفین-3Neurotrophin-4 - نوروتروفین-4Protein kinase C - پروتئین کیناز سیmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استCalphostin C - کالفوستین Cextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژنازtropomyosin receptor kinase - گیرپور کیناز تروپومیسین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Neurotrophin-induced neuroprotection against apoptosis was investigated using immature cultured cerebellar granule cells (CGC) from newborn rat pups. Apoptotic cell death induced by treatment with cytosine arabinoside (AraC) was confirmed by DNA fragmentation and quantified by cell survival assays. AraC was most effective in inducing apoptosis when added to CGC on the day of culture preparation, while less or no effect was observed when added at 24 or 48Â h after plating, respectively. Pretreatment of CGC cultures for 24Â h with brain-derived neurotrophic factor (BDNF) or neurotrophin-4 (NT-4), but not neurotrophin-3 (NT-3), robustly protected against AraC neurotoxicity. K252a, an inhibitor of the tropomyosin-related kinase (Trk) tyrosine kinase receptor family which showed no toxicity by itself, blocked BDNF protection of AraC-induced apoptosis in a concentration-dependent manner. Neither protein kinase C activation nor inhibition mimicked or affected BDNF protection against AraC neurotoxicity. BDNF, but not NT-3, treatment of immature CGC caused a marked, but transient activation of Akt through phosphatidylinositol (PI) 3-kinase. The neuroprotective effects of BDNF were suppressed by pretreatment with LY 294002 (a PI 3-kinase inhibitor). BDNF neuroprotection was also preceded by activation of mitogen activated protein kinase (MAPK) and suppressed by two MAPK/ERK (MEK)-selective inhibitors, PD 98059 and U-0126. Moreover, inhibitors of PI 3-kinase and MEK potentiated AraC-induced neurotoxicity. These results show that neurotrophins protect against AraC-induced apoptosis, at least in part, through TrkB-mediated activation of the PI 3-kinase/Akt and MEK signaling pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 46, Issue 1, January 2005, Pages 61-72
Journal: Neurochemistry International - Volume 46, Issue 1, January 2005, Pages 61-72
نویسندگان
P. Leeds, Y. Leng, E. Chalecka-Franaszek, D.-M. Chuang,