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10.1016/j.brainres.2010.10.084 http://scihub22266oqcxt.onion/10.1016/j.brainres.2010.10.084 21040713!ä!21040713 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21040713&cmd=llinks): Failed to open stream: HTTP request failed! 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Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels |pdf=|usr=}}{{21040713}} gab.com Text Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels JO: Brain Res http://www.kidney.de/pget.php?&tw=1&pmid=21040713 #FOAvip Mg(2+) is a known antagonist of some Ca(2+) ion channels. It may therefore be able to counteract the toxic consequences of excessive Ca(2+) entry into immune-type cells. Here we examined the effects of Mg(2+) on inflammation induced by Ca(2+) influx into microglia and THP-1 cells following activation of purinergic receptors. Using tissue culture, an inflammatory response was induced by treatment with either the P2X7 purinergic receptor agonist 2',3'-[benzoyl-4-benzoyl]-ATP (BzATP) or the P2Y2,4 receptor agonist uridine 5'-triphosphate (UTP). Both microglia and THP-1 cells expressed the mRNAs for these receptors. Treatment produced a rapid rise in intracellular Ca(2+) which was significantly reduced by Mg(2+) or the calcium chelator BAPTA-AM. Purinergic receptor stimulation activated the intracellular inflammatory pathway P38 MAP kinase and NFkappaB. This caused release of TNFalpha, IL-6, nitrite ions and other materials that are neurotoxic to SH-SY5Y cells. These effects were all ameliorated by Mg(2+). They were also partly ameliorated by the P2X7R antagonists, oxATP and KN-62, the P2YR antagonist MRS2179, and the store operated Ca(2+) channel blocker, SK96365. These results indicate that elevated Mg(2+) is a broad spectrum inhibitor of Ca(2+) entry into microglia or THP-1 cells. Mg(2+) administration may be a strategy for reducing the damaging consequences Ca(2+) induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease. Twit Text FOAVip Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels ????Brain Res http://www.kidney.de/pget.php?&tw=1&pmid=21040713 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21040713 #FOAvip English Wikipedia <ref>{{Cite pmid|21040713}}</ref> Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels #MMPMID21040713 Lee M; Jantaratnotai N; McGeer E; McLarnon JG; McGeer PL Brain Res 2011[Jan]; 1369 (ä): 21-35 PMID21040713show ga Mg(2+) is a known antagonist of some Ca(2+) ion channels. It may therefore be able to counteract the toxic consequences of excessive Ca(2+) entry into immune-type cells. Here we examined the effects of Mg(2+) on inflammation induced by Ca(2+) influx into microglia and THP-1 cells following activation of purinergic receptors. Using tissue culture, an inflammatory response was induced by treatment with either the P2X7 purinergic receptor agonist 2',3'-[benzoyl-4-benzoyl]-ATP (BzATP) or the P2Y2,4 receptor agonist uridine 5'-triphosphate (UTP). Both microglia and THP-1 cells expressed the mRNAs for these receptors. Treatment produced a rapid rise in intracellular Ca(2+) which was significantly reduced by Mg(2+) or the calcium chelator BAPTA-AM. Purinergic receptor stimulation activated the intracellular inflammatory pathway P38 MAP kinase and NFkappaB. This caused release of TNFalpha, IL-6, nitrite ions and other materials that are neurotoxic to SH-SY5Y cells. These effects were all ameliorated by Mg(2+). They were also partly ameliorated by the P2X7R antagonists, oxATP and KN-62, the P2YR antagonist MRS2179, and the store operated Ca(2+) channel blocker, SK96365. These results indicate that elevated Mg(2+) is a broad spectrum inhibitor of Ca(2+) entry into microglia or THP-1 cells. Mg(2+) administration may be a strategy for reducing the damaging consequences Ca(2+) induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease. |Blotting, Western[MESH] |Calcium/*metabolism[MESH] |Cell Line[MESH] |Humans[MESH] |Inflammation/metabolism/pathology/physiopathology[MESH] |Interleukin-6/biosynthesis[MESH] |Ions/metabolism[MESH] |Magnesium/*metabolism[MESH] |Microglia/drug effects/*metabolism/pathology[MESH] |Purinergic Agonists/pharmacology[MESH] |Receptors, Purinergic P2/metabolism[MESH] |Receptors, Purinergic P2X7/metabolism[MESH] |Receptors, Purinergic P2Y2/metabolism[MESH] |Reverse Transcriptase Polymerase Chain Reaction[MESH] |Signal Transduction/physiology[MESH]Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting(epmc).pdf DeepDyve Pubget Overpricing