کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10958491 | 1100075 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Distinct signaling pathways for induction of type II NOS by IFNγ and LPS in BV-2 microglial cells
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کلمات کلیدی
TNFα3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromidephorbol 12-myristate 13-acetateLPSDMEMPKCIκBNF-κBRAFNOSERKRASJanus kinase - کیناز جانوس BSA - BSADulbecco's modified Eagle Medium - Eagle Medium اصلاح شده DulbeccoPMA - LDC هاMAPK - MAPKMAPK kinase - MAPK کینازMTT - MTTbovine serum albumin - آلبومین سرم گاوSTAT - آمارinterferon - اینترفرونIFN - اینترفرون هاtumor necrosis factor α - تومور نکروز عامل αCNS - دستگاه عصبی مرکزیSerine/threonine kinase - سریین / ترئونین کینازMicroglial cells - سلول های میکروگلالیCytokine - سیتوکینcentral nervous system - سیستم عصبی مرکزیnuclear factor-κB - فاکتور هسته ای κBlipopolysaccharide - لیپوپلی ساکاریدsignal transducers and activators of transcription - مبدل سیگنال و فعال کننده رونویسیMEK - مجاهدین خلقNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازProtein kinase C - پروتئین کیناز سیmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenJAK - چگونهextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیGas - گاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Nitric oxide (NO) release upon microglial cell activation has been implicated in the tissue injury and cell death in many neurodegenerative diseases. Recent studies have indicated the ability of interferon-γ (IFNγ) and lipopolysaccharides (LPS) to independently induce type II nitric oxide synthase (iNOS) expression and NO production in BV-2 microglial cells. However, a detailed comparison between the signaling pathways activating iNOS by these two agents has not been accomplished. Analysis of PKC isoforms revealed mainly the presence of PKCδ, ι and λ in BV-2 cells. Although both IFNγ and LPS could specifically enhance the tyrosine phosphorylation of PKCδ, treatment with IFNγ induced a steady increase of phospho-PKCδ for up to 1 h, whereas treatment with LPS elevated phospho-PKCδ levels only transiently, with peak activity at 5 min. Rottlerin, a specific inhibitor for PKCδ, dose-dependently inhibited IFNγ- and LPS-induced NO production. Despite the common involvement of PKCδ, IFNγ- but not LPS-induced NO production involved extracellular signal-regulated kinases (ERK1/2) cascade and IFNγ-induced phosphorylation of ERK1/2 was mediated through PKC. On the other hand, LPS- but not IFNγ-induced NO production was through stimulation of NF-κB activation and nuclear translocation to interact with DNA. These results demonstrated distinct signaling pathways for induction of iNOS by IFNγ and LPS in BV-2 microglial cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 47, Issue 4, September 2005, Pages 298-307
Journal: Neurochemistry International - Volume 47, Issue 4, September 2005, Pages 298-307
نویسندگان
Siming Shen, Sue Yu, Joshua Binek, Malgorzata Chalimoniuk, Xiaolin Zhang, Shih-Ching Lo, Mark Hannink, Jinmei Wu, Kevin Fritsche, Rosario Donato, Grace Y. Sun,