کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6020597 | 1580410 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Potential role of A2A adenosine receptor in traumatic optic neuropathy
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
4-(2-[7-Amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenolZM241385NECACGS21680LPSMAPKinaseERK5′-N-ethylcarboxamidoadenosine - 5'-N-ethylcarboxamidoadenosineROS - ROSEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاTON - تنOxidative stress - تنش اکسیداتیوtumor necrosis factor-α - تومور نکروز عامل αInflammatory cytokines - سیتوکین های التهابیTNF-α - فاکتور نکروز توموری آلفاLipopolysaccharides - لیپوپلی ساکارید هاMicroglia - میکروگلیاهاTraumatic optic neuropathy - نوروپاتی اپتیکی تروماتیکmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenMAP kinase - کیناز MAPextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیReactive oxygen species - گونههای فعال اکسیژنAdenosine receptor - گیرنده آدنوزینAdenosine A2A receptor - گیرنده آدنوزین A2A
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
In traumatic optic neuropathy (TON), apoptosis of retinal ganglion cells is closely related to the local production of reactive oxygen species and inflammatory mediators from activated microglial cells. Adenosine receptor A2A (A2AAR) has been shown to possess anti-inflammatory properties that have not been studied in TON. In the present study, we examined the role of A2AAR in retinal complications associated with TON. Initial studies in wild-type mice revealed that treatment with the A2AAR agonist resulted in marked decreases in the TON-induced microglial activation, retinal cell death and releases of reactive oxygen species and pro-inflammatory cytokines TNF-α and IL-6. To further assess the role of A2AAR in TON, we studied the effects of A2AAR ablation on the TON-induced retinal abnormalities. A2AAR â/â mice with TON showed a significantly higher mRNA level of TNF-α, Iba1-1 in retinal tissue, and ICAM-1 expression in retinal sections compared with wild-type mice with TON. To explore a potential mechanism by which A2AAR-signaling regulates inflammation in TON, we performed additional studies using hypoxia- or LPS-treated microglial cells as an in vitro model for TON. Activation of A2AAR attenuates hypoxia or LPS-induced TNF-α release and significantly repressed the inflammatory signaling, ERK in the activated microglia. Collectively, this work provides pharmacological and genetic evidence for A2AAR signaling as a control point of cell death in TON and suggests that the retinal protective effect of A2AAR is mediated by attenuating the inflammatory response that occurs in microglia via interaction with MAPKinase pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 264, Issues 1â2, 15 November 2013, Pages 54-64
Journal: Journal of Neuroimmunology - Volume 264, Issues 1â2, 15 November 2013, Pages 54-64
نویسندگان
Saif Ahmad, Nadeem Fatteh, Nehal M. El-Sherbiny, Mohammad Naime, Ahmed S. Ibrahim, Ahmed M. El-Sherbini, Sally A. El-Shafey, Sohail Khan, Sadanand Fulzele, Joyce Gonzales, Gregory I. Liou,