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10.1016/j.brainres.2012.01.004 http://scihub22266oqcxt.onion/10.1016/j.brainres.2012.01.004 22297175!ä!22297175 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Brain+Res 2012 ; 1442 (ä): 1-8 Nephropedia Template TP {{tp|p=22297175|t=2012. Mechanisms of Mg2+ inhibition of BzATP-dependent Ca2+ responses in THP-1 monocytes |pdf=|usr=}}{{22297175}} gab.com Text Mechanisms of Mg2+ inhibition of BzATP-dependent Ca2+ responses in THP-1 monocytes JO: Brain Res http://www.kidney.de/pget.php?&tw=1&pmid=22297175 #FOAvip We have recently reported effects of Mg2+ to confer neuroprotection against toxicity of purinergic stimulated microglia and THP-1 monocytes. To examine mechanisms underlying neuroprotection, we have studied Mg2+ modulation of transient changes in intracellular Ca2+ ([Ca2+]i) in THP-1 cells induced by P2X7R agonist 2',3'-[benzoyl-4-benzoyl]-ATP (BzATP). Application of BzATP caused a rapid transient increase in [Ca2+]i followed by a prolonged component. The time course of the secondary slower phase was significantly reduced with Ca2+-free extracellular solution, with treatment of THP-1 cells by the P2X7R antagonist, oxATP or with exposure of cells to the store-operated channel (SOC) inhibitor, SKF96365. These results suggest that Ca2+ influx, mediated by both the P2X7R or by SOC, contribute to the slow component of [Ca2+]i. Treatment of THP-1 cells with 10 mMMg2+ was highly effective in reducing the time course of BzATP-induced Ca2+ decay; unlike the other modulatory protocols, Mg2+ markedly inhibited the amplitudes of slow and rapid components. In addition, acute application of Mg2+ during BzATP-induced responses elicited in the presence of either oxATP or SKF96365 to block respective P2X7R and SOC contributions, rapidly attenuated [Ca2+]i to baseline levels. Priming of cells with the inflammatory stimulus LPS/IFN-gamma markedly enhanced the slower, but not rapid, phase of BzATP-induced [Ca2+]i with application of 10 mMMg2+ inhibiting both components of response. A model is proposed to account for BzATP stimulation of both ionotropic P2XR and metabotropic P2YR which provides a mechanistic basis for elevated Mg2+ anti-inflammatory and neuroprotective actions in inflamed brain. Twit Text FOAVip Mechanisms of Mg2+ inhibition of BzATP-dependent Ca2+ responses in THP-1 monocytes ????Brain Res http://www.kidney.de/pget.php?&tw=1&pmid=22297175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22297175 #FOAvip English Wikipedia <ref>{{Cite pmid|22297175}}</ref> Mechanisms of Mg2+ inhibition of BzATP-dependent Ca2+ responses in THP-1 monocytes #MMPMID22297175 Jantaratnotai N; McGeer PL; McLarnon JG Brain Res 2012[Mar]; 1442 (ä): 1-8 PMID22297175show ga We have recently reported effects of Mg2+ to confer neuroprotection against toxicity of purinergic stimulated microglia and THP-1 monocytes. To examine mechanisms underlying neuroprotection, we have studied Mg2+ modulation of transient changes in intracellular Ca2+ ([Ca2+]i) in THP-1 cells induced by P2X7R agonist 2',3'-[benzoyl-4-benzoyl]-ATP (BzATP). Application of BzATP caused a rapid transient increase in [Ca2+]i followed by a prolonged component. The time course of the secondary slower phase was significantly reduced with Ca2+-free extracellular solution, with treatment of THP-1 cells by the P2X7R antagonist, oxATP or with exposure of cells to the store-operated channel (SOC) inhibitor, SKF96365. These results suggest that Ca2+ influx, mediated by both the P2X7R or by SOC, contribute to the slow component of [Ca2+]i. Treatment of THP-1 cells with 10 mMMg2+ was highly effective in reducing the time course of BzATP-induced Ca2+ decay; unlike the other modulatory protocols, Mg2+ markedly inhibited the amplitudes of slow and rapid components. In addition, acute application of Mg2+ during BzATP-induced responses elicited in the presence of either oxATP or SKF96365 to block respective P2X7R and SOC contributions, rapidly attenuated [Ca2+]i to baseline levels. Priming of cells with the inflammatory stimulus LPS/IFN-gamma markedly enhanced the slower, but not rapid, phase of BzATP-induced [Ca2+]i with application of 10 mMMg2+ inhibiting both components of response. A model is proposed to account for BzATP stimulation of both ionotropic P2XR and metabotropic P2YR which provides a mechanistic basis for elevated Mg2+ anti-inflammatory and neuroprotective actions in inflamed brain. |Adenosine Triphosphate/analogs & derivatives/metabolism/pharmacology[MESH] |Calcium/*metabolism[MESH] |Cell Line, Tumor[MESH] |Humans[MESH] |Imidazoles/pharmacology[MESH] |Interferon-gamma/immunology[MESH] |Lipopolysaccharides/immunology[MESH] |Magnesium/*pharmacology[MESH] |Models, Biological[MESH] |Monocytes/immunology/*metabolism[MESH] |Purinergic P2X Receptor Agonists/pharmacology[MESH] |Purinergic P2X Receptor Antagonists/pharmacology[MESH] |Receptors, Purinergic P2X7/metabolism[MESH]Mechanisms of Mg2+ inhibition of BzATP-dependent Ca2+ responses in THP(epmc).pdf DeepDyve Pubget Overpricing