کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9410777 | 1613317 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of the cyclooxygenase-2 system by interleukin-1β through mitogen-activated protein kinase signaling pathways: A comparative study of human neuroglioma and neuroblastoma cells
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Regulation of the cyclooxygenase-2 system by interleukin-1β through mitogen-activated protein kinase signaling pathways: A comparative study of human neuroglioma and neuroblastoma cells Regulation of the cyclooxygenase-2 system by interleukin-1β through mitogen-activated protein kinase signaling pathways: A comparative study of human neuroglioma and neuroblastoma cells](/preview/png/9410777.png)
چکیده انگلیسی
Glial activation and inflammation following brain injury may initiate and maintain the process of neurodegeneration. Both glia and neurons synthesize proinflammatory mediators such as interleukin 1 beta (IL-1β), cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2), and prostaglandins. The molecular mechanisms by which IL-1β regulates inflammatory genes such as cPLA2 and COX-2 in glial and neuronal cells are poorly understood. We have studied IL-1β-mediated gene regulation in an established glial and neuronal human cell lines. We report that IL-1β induced cPLA2 and COX-2 mRNA and protein expression and subsequent prostaglandin E2 (PGE2) release in a time-dependent manner in H4 neuroglioma cells. Both SB203580 and PD98059 [p38 and p42/44 mitogen-activated protein kinase (MAPKs) inhibitors, respectively] reduced IL-1β-induced PGE2 production, while only SB203580 reduced both cPLA2 and COX-2 expression. Similarly, in SKNSH neuroblastoma cells, both SB203580 and PD98059 reduced IL-1β-induced PGE2 release, with no detectable COX-2 and cPLA2 protein expression in these cells. Our results indicate that the signaling mechanisms of p38 and p42/44 MAPKs play a role in IL-1β-mediated PGE2 release in both of these cell lines, with differences upstream at the level of cPLA2/COX-2 expression. IL-1β-induced cPLA2 and COX-2 gene expression is modulated through the p38 MAPK pathway in both neuroglioma and neuroblastoma cells. Understanding the signaling mechanisms involved in IL-1β-mediated inflammatory processes in both glia and neuronal cells may provide potential targets for therapeutic intervention for neurological disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Brain Research - Volume 137, Issues 1â2, 13 June 2005, Pages 202-212
Journal: Molecular Brain Research - Volume 137, Issues 1â2, 13 June 2005, Pages 202-212
نویسندگان
Anju S. Moolwaney, Orisa J. Igwe,