کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738861 | 1046838 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of inducible nitric oxide synthase in proinflammatory cytokine-stimulated human primary astrocytes
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کلمات کلیدی
NF-κBEMSAd-NMMAL-NMMAAP-1IFN-γEAEiNOSRT-PCRIL-1DMEMc/ebpβ - c / ebpβDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoHuman astrocytes - آستروسیت های انسانیexperimental allergic encephalomyelitis - آنسفالومیلیت آلرژیک تجربیinterferon-γ - اینترفرون-γinterleukin-1 - اینترلوکین-1electrophoretic mobility-shift assay - تحرک انتقال الکتریکی - تحرک تغییرtumor necrosis factor-α - تومور نکروز عامل αCNS - دستگاه عصبی مرکزیTNF-α - فاکتور نکروز توموری آلفاCerebrospinal fluid - مایع مغزی نخاعیCSF - مایع مغزی نخاعیMultiple sclerosis - مولتیپل اسکلروزیس(ام اس)real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیGas - گاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The present study was undertaken to investigate the mechanism of expression of inducible nitric oxide synthase (iNOS) in human primary astrocytes. Among IL-1β, TNF-α, and IFN-γ, only IL-1β alone was capable of inducing iNOS. Similarly, among different cytokine combinations, the combinations involving only IL-1β as a partner were capable of inducing iNOS. The combination of IL-1β and IFN-γ (IL-IF) induced the expression of iNOS at the highest level. All three cytokines alone induced the activation of AP-1 while IL-1β and TNF-α but not IFN-γ induced the activation of NF-κB. However, among the three cytokines, only IL-1β was capable of inducing the activation of CCAAT/enhancer-binding proteinβ (C/EBPβ), suggesting an essential role of C/EBPβ in the expression of iNOS in astrocytes. Although IL-1β and IFN-γ alone induced the activation of AP-1, the combination of these two cytokines (IL-IF) markedly inhibited the activation of AP-1. Consistently, JNK-I, a specific inhibitor of JNK, inhibited IL-1β-mediated activation of AP-1 and expression of iNOS. On the other hand, JNK-I had no effect on (IL-IF)-induced expression of iNOS, suggesting that the activation of AP-1 is involved only during the low level of iNOS induction by IL-1β but not during the high level of induction by IL-IF. In contrast, the activation of γ-activation site (GAS) was involved only during the high level of induction by IL-IF but not during the low level of induction by IL-1β. However, the activation of NF-κB and C/EBPβ was involved in the induction of iNOS by IL-1β as well as by IL-IF.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 5, 1 March 2005, Pages 655-664
Journal: Free Radical Biology and Medicine - Volume 38, Issue 5, 1 March 2005, Pages 655-664
نویسندگان
Malabendu Jana, Jamar A. Anderson, Ramendra N. Saha, Xiaojuan Liu, Kalipada Pahan,