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10.1371/journal.pone.0236361 http://scihub22266oqcxt.onion/10.1371/journal.pone.0236361 32706793!7380890!32706793     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2020 ; 15 (7): e0236361 Nephropedia Template TP {{tp|p=32706793|t=2020. Elevated serum magnesium lowers calcification propensity in Memo1-deficient mice |pdf=|usr=}}{{32706793}} gab.com Text Elevated serum magnesium lowers calcification propensity in Memo1-deficient mice JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=32706793 #FOAvip MEdiator of cell MOtility1 (MEMO1) is a ubiquitously expressed redox protein involved in extracellular ligand-induced cell signaling. We previously reported that inducible whole-body Memo1 KO (cKO) mice displayed a syndrome of premature aging and disturbed mineral metabolism partially recapitulating the phenotype observed in Klotho or Fgf23-deficient mouse models. Here, we aimed at delineating the contribution of systemic mineral load on the Memo1 cKO mouse phenotype. We attempted to rescue the Memo1 cKO phenotype by depleting phosphate or vitamin D from the diet, but did not observe any effect on survival. However, we noticed that, by contrast to Klotho or Fgf23-deficient mouse models, Memo1 cKO mice did not present any soft-tissue calcifications and displayed even a decreased serum calcification propensity. We identified higher serum magnesium levels as the main cause of protection against calcifications. Expression of genes encoding intestinal and renal magnesium channels and the regulator epidermal growth factor were increased in Memo1 cKO. In order to check whether magnesium reabsorption in the kidney alone was driving the higher magnesemia, we generated a kidney-specific Memo1 KO (kKO) mouse model. Memo1 kKO mice also displayed higher magnesemia and increased renal magnesium channel gene expression. Collectively, these data identify MEMO1 as a novel regulator of magnesium homeostasis and systemic calcification propensity, by regulating expression of the main magnesium channels. Twit Text FOAVip Elevated serum magnesium lowers calcification propensity in Memo1-deficient mice ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=32706793 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32706793 #FOAvip English Wikipedia <ref>{{Cite pmid|32706793}}</ref> Elevated serum magnesium lowers calcification propensity in Memo1-deficient mice #MMPMID32706793 Moor MB; Ramakrishnan SK; Legrand F; Bachtler M; Koesters R; Hynes NE; Pasch A; Bonny O PLoS One 2020[]; 15 (7): e0236361 PMID32706793show ga MEdiator of cell MOtility1 (MEMO1) is a ubiquitously expressed redox protein involved in extracellular ligand-induced cell signaling. We previously reported that inducible whole-body Memo1 KO (cKO) mice displayed a syndrome of premature aging and disturbed mineral metabolism partially recapitulating the phenotype observed in Klotho or Fgf23-deficient mouse models. Here, we aimed at delineating the contribution of systemic mineral load on the Memo1 cKO mouse phenotype. We attempted to rescue the Memo1 cKO phenotype by depleting phosphate or vitamin D from the diet, but did not observe any effect on survival. However, we noticed that, by contrast to Klotho or Fgf23-deficient mouse models, Memo1 cKO mice did not present any soft-tissue calcifications and displayed even a decreased serum calcification propensity. We identified higher serum magnesium levels as the main cause of protection against calcifications. Expression of genes encoding intestinal and renal magnesium channels and the regulator epidermal growth factor were increased in Memo1 cKO. In order to check whether magnesium reabsorption in the kidney alone was driving the higher magnesemia, we generated a kidney-specific Memo1 KO (kKO) mouse model. Memo1 kKO mice also displayed higher magnesemia and increased renal magnesium channel gene expression. Collectively, these data identify MEMO1 as a novel regulator of magnesium homeostasis and systemic calcification propensity, by regulating expression of the main magnesium channels. |Animals[MESH] |Calcinosis/genetics/*metabolism[MESH] |Female[MESH] |Fibroblast Growth Factor-23[MESH] |Homeostasis[MESH] |Intracellular Signaling Peptides and Proteins/*deficiency/genetics[MESH] |Ion Channels/metabolism[MESH] |Kidney/*metabolism[MESH] |Magnesium/*blood[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Phosphates/metabolism[MESH]Elevated serum magnesium lowers calcification propensity in Memo1-defi(epmc).pdf DeepDyve Pubget Overpricing