کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8478866 | 1551257 | 2018 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of the ARE-binding proteins, TTP (tristetraprolin) and HuR (human antigen R), in inflammatory response in astrocytes
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کلمات کلیدی
TNFαFGLhuman antigen RPGNTTPTLRp38PPARPGE2FlagellinNF-κBLPSDMEMJnkMAPK - MAPKDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoMitogen activated protein kinases - Mitogen فعال پروتئین کینازp38 MAPK - P38 MAPKAstrocytes - آستروسیتinflammation - التهاب( توروم) interleukin - اینترلوکینMRNA degradation - تخریب MRNATristetraprolin - تریسترا پرولینtumor necrosis factor α - تومور نکروز عامل αcycloheximide - سیکلوهایسیمیدcyclooxygenase 2 - سیکلوکوکسیژناز 2nuclear factor kappa-light-chain-enhancer of activated B cells - فاکتور هسته ای kappa-light-chain-enhancer از سلول های B فعال شده استlipopolysaccharide - لیپوپلی ساکاریدARE - هستندp38 mitogen-activated protein kinases - پروتئین کیناز متیوژن فعال P38Prostaglandin E2 - پروستاگلاندین E2Peptidoglycan - پپتیدوگلیکانHuR - چگونهperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیومToll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Control of decay of mRNA containing the adenine-uridine rich elements (AREs) is an important post-transcriptional mechanism involved in the regulation of inflammatory gene expression. Two widely recognized proteins in this machinery are HuR (human antigen R) - a protein that stabilizes ARE-containing mRNA and TTP (tristetraprolin) - a protein that shortens half-lives of ARE-containing mRNA. Although HuR and TTP regulation mechanisms have been well studied in cells of hematopoietic origin, there are no respective data in astrocytes, cells of ectodermal origin which play an important role in neuroinflammation. Therefore we evaluated the existence of TTP and HuR in primary astrocytes and characterized the features of their regulation after stimulation by the proinflammatory stimuli thrombin, ATP, and agonists of TLR4, TLR2. All proinflammatory stimuli increased levels of TTP mRNA, but not HuR mRNA. Transcripts of both HuR and TTP underwent stabilization upon lipopolysaccharide (LPS) treatment, measured with the actinomycin D protocol. This effect was abolished by treatment with SB203580, an inhibitor of Ñ38 ÐÐÐ Ð. Both TTP and HuR transcripts were sensitive to modulation by anisomycin and cycloheximide. LPS induced translocation of HuR protein from nucleus to cytoplasm. TTP is localized in the cytosolic fraction and localization is not sensitive to LPS treatment. Our data for the first time reveal specificity of regulation of ARE-binding proteins in astrocytes. We propose possibilities to manipulate brain inflammatory processes via post-transcription regulatory steps in astrocytes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 118, September 2018, Pages 82-90
Journal: Neurochemistry International - Volume 118, September 2018, Pages 82-90
نویسندگان
Alina A. Astakhova, Dmitry V. Chistyakov, Marina G. Sergeeva, Georg Reiser,