Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Signaling pathways mediating a selective induction of nitric oxide synthase II by tumor necrosis factor alpha in nerve growth factor-responsive cells | Journal of Neuroinflammation BioMed Central Research Open Access Signaling pathways mediating a selective induction of nitric oxide synthase II by tumor necrosis factor alpha in nerve growth factor-responsive cells Michael S Thomas1 WenRu Zhang1 Paivi M Jordan1 H Uri Saragovi2 and Giulio Taglialatela 1 Address Department of Neuroscience and Cell Biology the University of Texas Medical Branch at Galveston Texas - USA and 2Department of Pharmacology and Therapeutics McGill University Montreal QC Canada Email Michael S Thomas - msthomas@ WenRu Zhang - wezhang@ Paivi M Jordan - pmroozen@ H Uri Saragovi - Giulio Taglialatela - gtaglial@ Corresponding author Published 06 September 2005 Received 10 March 2005 Journal ofNeuroinflammation 2005 2 19 doi l742-2094-2-l9 Accepted 06 September 2005 This article is available from http content 2 l l9 2005 Thomas et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Inflammation and oxidative stress play a critical role in neurodegeneration associated with acute and chronic insults of the nervous system. Notably affected neurons are often responsive to and dependent on trophic factors such as nerve growth factor NGF . We previously showed in NGF-responsive PCl2 cells that tumor necrosis factor alpha TNFa and NGF synergistically induce the expression of the free-radical producing enzyme inducible nitric oxide synthase iNOS . We proposed that NGF-responsive neurons might be selectively exposed to iNOS-mediated oxidative damage as a consequence of elevated TNFa levels. With the aim of identifying possible therapeutic targets in the present study we investigated the signaling pathways .
