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10.1074/jbc.M115.696781 http://scihub22266oqcxt.onion/10.1074/jbc.M115.696781 C4938171!4938171!27226532     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 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       J+Biol+Chem 2016 ; 291 (28): 14468-82 Nephropedia Template TP {{tp|p=27226532|t=2016. Genetic Ablation of Calcium-independent Phospholipase A2? Induces Glomerular Injury in Mice* |pdf=|usr=}}{{27226532}} gab.com Text Genetic Ablation of Calcium-independent Phospholipase A2 Induces Glomerular Injury in Mice* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27226532 #FOAvip Glomerular visceral epithelial cells (podocytes) play a critical role in the maintenance of glomerular permselectivity. Podocyte injury, manifesting as proteinuria, is the cause of many glomerular diseases. We reported previously that calcium-independent phospholipase A2? (iPLA2?) is cytoprotective against complement-mediated glomerular epithelial cell injury. Studies in iPLA2? KO mice have demonstrated an important role for iPLA2? in mitochondrial lipid turnover, membrane structure, and metabolism. The aim of the present study was to employ iPLA2? KO mice to better understand the role of iPLA2? in normal glomerular and podocyte function as well as in glomerular injury. We show that deletion of iPLA2? did not cause detectable albuminuria; however, it resulted in mitochondrial structural abnormalities and enhanced autophagy in podocytes as well as loss of podocytes in aging KO mice. Moreover, after induction of anti-glomerular basement membrane nephritis in young mice, iPLA2? KO mice exhibited significantly increased levels of albuminuria, podocyte injury, and loss of podocytes compared with wild type. Thus, iPLA2? has a protective functional role in the normal glomerulus and in glomerulonephritis. Understanding the role of iPLA2? in glomerular pathophysiology provides opportunities for the development of novel therapeutic approaches to glomerular injury and proteinuria. Twit Text FOAVip Genetic Ablation of Calcium-independent Phospholipase A2 Induces Glomerular Injury in Mice* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27226532 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27226532 #FOAvip English Wikipedia <ref>{{Cite pmid|27226532}}</ref> Genetic Ablation of Calcium-independent Phospholipase A2? Induces Glomerular Injury in Mice* #MMPMID27226532 Elimam H; Papillon J; Kaufman DR; Guillemette J; Aoudjit L; Gross RW; Takano T; Cybulsky AV J Biol Chem 2016[Jul]; 291 (28): 14468-82 PMID27226532show ga Glomerular visceral epithelial cells (podocytes) play a critical role in the maintenance of glomerular permselectivity. Podocyte injury, manifesting as proteinuria, is the cause of many glomerular diseases. We reported previously that calcium-independent phospholipase A2? (iPLA2?) is cytoprotective against complement-mediated glomerular epithelial cell injury. Studies in iPLA2? KO mice have demonstrated an important role for iPLA2? in mitochondrial lipid turnover, membrane structure, and metabolism. The aim of the present study was to employ iPLA2? KO mice to better understand the role of iPLA2? in normal glomerular and podocyte function as well as in glomerular injury. We show that deletion of iPLA2? did not cause detectable albuminuria; however, it resulted in mitochondrial structural abnormalities and enhanced autophagy in podocytes as well as loss of podocytes in aging KO mice. Moreover, after induction of anti-glomerular basement membrane nephritis in young mice, iPLA2? KO mice exhibited significantly increased levels of albuminuria, podocyte injury, and loss of podocytes compared with wild type. Thus, iPLA2? has a protective functional role in the normal glomerulus and in glomerulonephritis. Understanding the role of iPLA2? in glomerular pathophysiology provides opportunities for the development of novel therapeutic approaches to glomerular injury and proteinuria. äGenetic Ablation of Calcium-independent Phospholipase A2? Induces Glom(epmc).pdf DeepDyve Pubget Overpricing