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10.1038/s41374-019-0304-z http://scihub22266oqcxt.onion/10.1038/s41374-019-0304-z 31444399!ä!31444399 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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Lab+Invest 2020 ; 100 (2): 234-249 Nephropedia Template TP {{tp|p=31444399|t=2020. TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia |pdf=|usr=}}{{31444399}} gab.com Text TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia JO: Lab Invest http://www.kidney.de/pget.php?&tw=1&pmid=31444399 #FOAvip Sepsis is the main cause of mortality in patients admitted to intensive care units. During sepsis, endothelial permeability is severely augmented, contributing to renal dysfunction and patient mortality. Ca(2+) influx and the subsequent increase in intracellular [Ca(2+)](i) in endothelial cells (ECs) are key steps in the establishment of endothelial hyperpermeability. Transient receptor potential melastatin 7 (TRPM7) ion channels are permeable to Ca(2+) and are expressed in a broad range of cell types and tissues, including ECs and kidneys. However, the role of TRPM7 on endothelial hyperpermeability during sepsis has remained elusive. Therefore, we investigated the participation of TRPM7 in renal vascular hyperpermeability, renal dysfunction, and enhanced mortality induced by endotoxemia. Our results showed that endotoxin increases endothelial hyperpermeability and Ca(2+) overload through the TLR4/NOX-2/ROS/NF-kappaB pathway. Moreover, endotoxin exposure was shown to downregulate the expression of VE-cadherin, compromising monolayer integrity and enhancing vascular hyperpermeability. Notably, endotoxin-induced endothelial hyperpermeability was substantially inhibited by pharmacological inhibition and specific suppression of TRPM7 expression. The endotoxin was shown to upregulate the expression of TRPM7 via the TLR4/NOX-2/ROS/NF-kappaB pathway and induce a TRPM7-dependent EC Ca(2+) overload. Remarkably, in vivo experiments performed in endotoxemic animals showed that pharmacological inhibition and specific suppression of TRPM7 expression inhibits renal vascular hyperpermeability, prevents kidney dysfunction, and improves survival in endotoxemic animals. Therefore, our results showed that TRPM7 mediates endotoxemia-induced endothelial hyperpermeability, renal dysfunction, and enhanced mortality, revealing a novel molecular target for treating renal vascular hyperpermeability and kidney dysfunction during endotoxemia, sepsis, and other inflammatory diseases. Twit Text FOAVip TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia ????Lab Invest http://www.kidney.de/pget.php?&tw=1&pmid=31444399 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31444399 #FOAvip English Wikipedia <ref>{{Cite pmid|31444399}}</ref> TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia #MMPMID31444399 Gatica S; Villegas V; Vallejos A; Olivares P; Aballai V; Lagos-Meza F; Echeverria C; Cabello-Verrugio C; Varela D; Simon F Lab Invest 2020[Feb]; 100 (2): 234-249 PMID31444399show ga Sepsis is the main cause of mortality in patients admitted to intensive care units. During sepsis, endothelial permeability is severely augmented, contributing to renal dysfunction and patient mortality. Ca(2+) influx and the subsequent increase in intracellular [Ca(2+)](i) in endothelial cells (ECs) are key steps in the establishment of endothelial hyperpermeability. Transient receptor potential melastatin 7 (TRPM7) ion channels are permeable to Ca(2+) and are expressed in a broad range of cell types and tissues, including ECs and kidneys. However, the role of TRPM7 on endothelial hyperpermeability during sepsis has remained elusive. Therefore, we investigated the participation of TRPM7 in renal vascular hyperpermeability, renal dysfunction, and enhanced mortality induced by endotoxemia. Our results showed that endotoxin increases endothelial hyperpermeability and Ca(2+) overload through the TLR4/NOX-2/ROS/NF-kappaB pathway. Moreover, endotoxin exposure was shown to downregulate the expression of VE-cadherin, compromising monolayer integrity and enhancing vascular hyperpermeability. Notably, endotoxin-induced endothelial hyperpermeability was substantially inhibited by pharmacological inhibition and specific suppression of TRPM7 expression. The endotoxin was shown to upregulate the expression of TRPM7 via the TLR4/NOX-2/ROS/NF-kappaB pathway and induce a TRPM7-dependent EC Ca(2+) overload. Remarkably, in vivo experiments performed in endotoxemic animals showed that pharmacological inhibition and specific suppression of TRPM7 expression inhibits renal vascular hyperpermeability, prevents kidney dysfunction, and improves survival in endotoxemic animals. Therefore, our results showed that TRPM7 mediates endotoxemia-induced endothelial hyperpermeability, renal dysfunction, and enhanced mortality, revealing a novel molecular target for treating renal vascular hyperpermeability and kidney dysfunction during endotoxemia, sepsis, and other inflammatory diseases. |*Endotoxemia/metabolism/mortality[MESH] |Animals[MESH] |Capillary Permeability/*physiology[MESH] |Cell Line[MESH] |Endothelium, Vascular/*metabolism/physiopathology[MESH] |Human Umbilical Vein Endothelial Cells[MESH] |Humans[MESH] |Kidney Diseases/*metabolism/physiopathology[MESH] |Kidney/metabolism/physiopathology[MESH] |Male[MESH] |Protein Serine-Threonine Kinases/genetics/metabolism[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH] |Signal Transduction/physiology[MESH]TRPM7 mediates kidney injury, endothelial hyperpermeability and mortal(epmc).pdf DeepDyve Pubget Overpricing