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10.1002/jnr.22748 http://scihub22266oqcxt.onion/10.1002/jnr.22748 C3218197!3218197 !21932365     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21932365 &cmd=llinks): Failed to open stream: HTTP request failed! 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Neutral sphingomyelinase activation precedes NADPH oxidase-dependent damage in neurons exposed to the proinflammatory cytokine tumor necrosis factor-? |pdf=|usr=}}{{21932365 }} gab.com Text Neutral sphingomyelinase activation precedes NADPH oxidase-dependent damage in neurons exposed to the proinflammatory cytokine tumor necrosis factor- JO: J Neurosci Res http://www.kidney.de/pget.php?&tw=1&pmid=21932365 #FOAvip Inflammation accompanied by severe oxidative stress plays a vital role in the orchestration and progression of neurodegeneration prevalent in chronic and acute central nervous system pathologies as well as in aging. The proinflammatory cytokine tumor necrosis factor-? (TNF?) elicits the formation of the bioactive ceramide by stimulating the hydrolysis of the membrane lipid sphingomyelin by sphingomyelinase activities. Ceramide stimulates the formation of reactive oxygen species (ROS) and apoptotic mechanisms in both neurons and nonneuronal cells, establishing a link between sphingolipid metabolism and oxidative stress. We demonstrated in SH-SY5Y human neuroblastoma cells and primary cortical neurons that TNF? is a potent stimulator of Mg(2+) -dependent neutral sphingomyelinase (Mg(2+) -nSMase) activity, and sphingomyelin hydrolysis, rather than de novo synthesis, was the predominant source of ceramide increases. Mg(2+) -nSMase activity preceded an accumulation of ROS by a neuronal NADPH oxidase (NOX). Notably, TNF? provoked an NOX-dependent oxidative damage to sphingosine kinase-1, which generates sphingosine-1-phosphate, a ceramide metabolite associated with neurite outgrowth. Indeed, ceramide and ROS inhibited neurite outgrowth of dorsal root ganglion neurons by disrupting growth cone motility. Blunting ceramide and ROS formation both rescued sphingosine kinase-1 activity and neurite outgrowth. Our studies suggest that TNF?-mediated activation of Mg(2+) -nSMase and NOX in neuronal cells not only produced the neurotoxic intermediates ceramide and ROS but also directly antagonized neuronal survival mechanisms, thus accelerating neurodegeneration. Twit Text FOAVip Neutral sphingomyelinase activation precedes NADPH oxidase-dependent damage in neurons exposed to the proinflammatory cytokine tumor necrosis factor- ????J Neurosci Res http://www.kidney.de/pget.php?&tw=1&pmid=21932365 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21932365 #FOAvip English Wikipedia <ref>{{Cite pmid|21932365 }}</ref> Neutral sphingomyelinase activation precedes NADPH oxidase-dependent damage in neurons exposed to the proinflammatory cytokine tumor necrosis factor-? #MMPMID21932365 Barth BM ; Gustafson SJ ; Kuhn TB J Neurosci Res 2012[Jan]; 90 (1 ): 229-42 PMID21932365 show ga Inflammation accompanied by severe oxidative stress plays a vital role in the orchestration and progression of neurodegeneration prevalent in chronic and acute central nervous system pathologies as well as in aging. The proinflammatory cytokine tumor necrosis factor-? (TNF?) elicits the formation of the bioactive ceramide by stimulating the hydrolysis of the membrane lipid sphingomyelin by sphingomyelinase activities. Ceramide stimulates the formation of reactive oxygen species (ROS) and apoptotic mechanisms in both neurons and nonneuronal cells, establishing a link between sphingolipid metabolism and oxidative stress. We demonstrated in SH-SY5Y human neuroblastoma cells and primary cortical neurons that TNF? is a potent stimulator of Mg(2+) -dependent neutral sphingomyelinase (Mg(2+) -nSMase) activity, and sphingomyelin hydrolysis, rather than de novo synthesis, was the predominant source of ceramide increases. Mg(2+) -nSMase activity preceded an accumulation of ROS by a neuronal NADPH oxidase (NOX). Notably, TNF? provoked an NOX-dependent oxidative damage to sphingosine kinase-1, which generates sphingosine-1-phosphate, a ceramide metabolite associated with neurite outgrowth. Indeed, ceramide and ROS inhibited neurite outgrowth of dorsal root ganglion neurons by disrupting growth cone motility. Blunting ceramide and ROS formation both rescued sphingosine kinase-1 activity and neurite outgrowth. Our studies suggest that TNF?-mediated activation of Mg(2+) -nSMase and NOX in neuronal cells not only produced the neurotoxic intermediates ceramide and ROS but also directly antagonized neuronal survival mechanisms, thus accelerating neurodegeneration. |Animals [MESH] |Apoptosis/drug effects [MESH] |Cell Membrane/drug effects/metabolism [MESH] |Ceramides [MESH] |Cerebral Cortex/cytology [MESH] |Chick Embryo [MESH] |Drug Interactions [MESH] |Enzyme Inhibitors/pharmacology [MESH] |Growth Cones/drug effects/physiology [MESH] |Humans [MESH] |Magnesium/metabolism [MESH] |NADPH Oxidases/*metabolism [MESH] |Neurites/drug effects/physiology [MESH] |Neuroblastoma/pathology [MESH] |Neurons/cytology/*drug effects/*enzymology [MESH] |Palmitates/pharmacology [MESH] |Phosphotransferases (Alcohol Group Acceptor)/metabolism [MESH] |RNA, Small Interfering/pharmacology [MESH] |Reactive Oxygen Species [MESH] |Sphingomyelin Phosphodiesterase/*metabolism [MESH]Neutral sphingomyelinase activation precedes NADPH oxidase-dependent d(epmc).pdf DeepDyve Pubget Overpricing