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10.1007/s12035-019-01713-7 http://scihub22266oqcxt.onion/10.1007/s12035-019-01713-7 31392516!6968994!31392516     free     free     free 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       Mol+Neurobiol 2020 ; 57 (1): 528-538 Nephropedia Template TP {{tp|p=31392516|t=2020. Magnesium-Induced Cell Survival Is Dependent on TRPM7 Expression and Function |pdf=|usr=}}{{31392516}} gab.com Text Magnesium-Induced Cell Survival Is Dependent on TRPM7 Expression and Function JO: Mol Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=31392516 #FOAvip Mg(2+) homeostasis is essential for cell survival and the loss of this regulation has been associated with many neurodegenerative diseases, including loss of dopaminergic neurons. Although the neurotoxin-mediated loss of dopaminergic neurons in Parkinson disease models is extensively studied, the ion channel(s) that regulate Mg(2+) homeostasis and thus could prevent neuronal cell death is not yet identified. Here, we show that TRPM7 (transient receptor potential melastatin 7) is involved in regulating Mg(2+) homeostasis in dopaminergic cells. Importantly, transient loss of TRPM7 decreased intracellular Mg(2+) levels and decreased dopaminergic cells/neurons survival. We provide further evidence that both increases in extracellular Mg(2+) or transiently increasing TRPM7 levels protected dopaminergic SH-SY5Y cells against neurotoxin-mediated cell death. Neurotoxin treatment significantly decreased TRPM7 levels in both SH-SY5Y cells and the substantia nigra pars compacta region of mice, along with a decrease in Mg(2+) influx. Moreover, Mg(2+) supplementation showed a concentration-dependent decrease in caspase-3 activity, an increase in cell survival, restored mitochondrial membrane potential, and increase TRPM7 levels in neurotoxin-treated cells. In contrast, transient silencing of TRPM7 inhibited the positive effect of Mg(2+) supplementation in protecting against neurotoxins. Whereas, TRPM7 overexpression not only maintained Mg(2+) homeostasis but also inhibited caspase 3 activity that induced cell survival. Overall, these results suggest a significant role of TRPM7 channels in Mg(2+) homeostasis and the survival of neurotoxin-induced loss of dopaminergic cells. Twit Text FOAVip Magnesium-Induced Cell Survival Is Dependent on TRPM7 Expression and Function ????Mol Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=31392516 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31392516 #FOAvip English Wikipedia <ref>{{Cite pmid|31392516}}</ref> Magnesium-Induced Cell Survival Is Dependent on TRPM7 Expression and Function #MMPMID31392516 Sun Y; Sukumaran P; Singh BB Mol Neurobiol 2020[Jan]; 57 (1): 528-538 PMID31392516show ga Mg(2+) homeostasis is essential for cell survival and the loss of this regulation has been associated with many neurodegenerative diseases, including loss of dopaminergic neurons. Although the neurotoxin-mediated loss of dopaminergic neurons in Parkinson disease models is extensively studied, the ion channel(s) that regulate Mg(2+) homeostasis and thus could prevent neuronal cell death is not yet identified. Here, we show that TRPM7 (transient receptor potential melastatin 7) is involved in regulating Mg(2+) homeostasis in dopaminergic cells. Importantly, transient loss of TRPM7 decreased intracellular Mg(2+) levels and decreased dopaminergic cells/neurons survival. We provide further evidence that both increases in extracellular Mg(2+) or transiently increasing TRPM7 levels protected dopaminergic SH-SY5Y cells against neurotoxin-mediated cell death. Neurotoxin treatment significantly decreased TRPM7 levels in both SH-SY5Y cells and the substantia nigra pars compacta region of mice, along with a decrease in Mg(2+) influx. Moreover, Mg(2+) supplementation showed a concentration-dependent decrease in caspase-3 activity, an increase in cell survival, restored mitochondrial membrane potential, and increase TRPM7 levels in neurotoxin-treated cells. In contrast, transient silencing of TRPM7 inhibited the positive effect of Mg(2+) supplementation in protecting against neurotoxins. Whereas, TRPM7 overexpression not only maintained Mg(2+) homeostasis but also inhibited caspase 3 activity that induced cell survival. Overall, these results suggest a significant role of TRPM7 channels in Mg(2+) homeostasis and the survival of neurotoxin-induced loss of dopaminergic cells. |1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine[MESH] |Animals[MESH] |Apoptosis/drug effects[MESH] |Autophagy/drug effects[MESH] |Cell Line, Tumor[MESH] |Cell Survival/drug effects[MESH] |Dopaminergic Neurons/drug effects/metabolism[MESH] |Magnesium/*pharmacology[MESH] |Male[MESH] |Mice, Inbred C57BL[MESH] |Neurotoxins/toxicity[MESH]Magnesium-Induced Cell Survival Is Dependent on TRPM7 Expression and F(epmc).pdf DeepDyve Pubget Overpricing