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10.1152/ajprenal.00608.2013 http://scihub22266oqcxt.onion/10.1152/ajprenal.00608.2013 C4042102!4042102 !24598802     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24598802 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mpv17 in mitochondria protects podocytes against mitochondrial dysfunction and apoptosis in vivo and in vitro |pdf=|usr=}}{{24598802 }} gab.com Text Mpv17 in mitochondria protects podocytes against mitochondrial dysfunction and apoptosis in vivo and in vitro JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24598802 #FOAvip Mitochondrial dysfunction is increasingly recognized as contributing to glomerular diseases, including those secondary to mitochondrial DNA (mtDNA) mutations and deletions. Mitochondria maintain cellular redox and energy homeostasis and are a major source of intracellular reactive oxygen species (ROS) production. Mitochondrial ROS accumulation may contribute to stress-induced mitochondrial dysfunction and apoptosis and thereby to glomerulosclerosis. In mice, deletion of the gene encoding Mpv17 is associated with glomerulosclerosis, but the underlying mechanism remains poorly defined. Here we report that Mpv17 localizes to mitochondria of podocytes and its expression is reduced in several glomerular injury models and in human focal segmental glomerulosclerosis (FSGS) but not in minimal change disease. Using models of mild or severe nephrotoxic serum nephritis (NTSN) in Mpv17(+/+) wild-type (WT) and Mpv17(-/-) knockout mice, we found that Mpv17 deficiency resulted in increased proteinuria (mild NTSN) and renal insufficiency (severe NTSN) compared with WT. These lesions were associated with increased mitochondrial ROS generation and mitochondrial injury such as oxidative DNA damage. In vitro, podocytes with loss of Mpv17 function were characterized by increased susceptibility to apoptosis and ROS injury including decreased mitochondrial function, loss of mtDNA content, and change in mitochondrial configuration. In summary, the inner mitochondrial membrane protein Mpv17 in podocytes is essential for the maintenance of mitochondrial homeostasis and protects podocytes against oxidative stress-induced injury both in vitro and in vivo. Twit Text FOAVip Mpv17 in mitochondria protects podocytes against mitochondrial dysfunction and apoptosis in vivo and in vitro ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24598802 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24598802 #FOAvip English Wikipedia <ref>{{Cite pmid|24598802 }}</ref> Mpv17 in mitochondria protects podocytes against mitochondrial dysfunction and apoptosis in vivo and in vitro #MMPMID24598802 Casalena G ; Krick S ; Daehn I ; Yu L ; Ju W ; Shi S ; Tsai SY ; D'Agati V ; Lindenmeyer M ; Cohen CD ; Schlondorff D ; Bottinger EP Am J Physiol Renal Physiol 2014[Jun]; 306 (11 ): F1372-80 PMID24598802 show ga Mitochondrial dysfunction is increasingly recognized as contributing to glomerular diseases, including those secondary to mitochondrial DNA (mtDNA) mutations and deletions. Mitochondria maintain cellular redox and energy homeostasis and are a major source of intracellular reactive oxygen species (ROS) production. Mitochondrial ROS accumulation may contribute to stress-induced mitochondrial dysfunction and apoptosis and thereby to glomerulosclerosis. In mice, deletion of the gene encoding Mpv17 is associated with glomerulosclerosis, but the underlying mechanism remains poorly defined. Here we report that Mpv17 localizes to mitochondria of podocytes and its expression is reduced in several glomerular injury models and in human focal segmental glomerulosclerosis (FSGS) but not in minimal change disease. Using models of mild or severe nephrotoxic serum nephritis (NTSN) in Mpv17(+/+) wild-type (WT) and Mpv17(-/-) knockout mice, we found that Mpv17 deficiency resulted in increased proteinuria (mild NTSN) and renal insufficiency (severe NTSN) compared with WT. These lesions were associated with increased mitochondrial ROS generation and mitochondrial injury such as oxidative DNA damage. In vitro, podocytes with loss of Mpv17 function were characterized by increased susceptibility to apoptosis and ROS injury including decreased mitochondrial function, loss of mtDNA content, and change in mitochondrial configuration. In summary, the inner mitochondrial membrane protein Mpv17 in podocytes is essential for the maintenance of mitochondrial homeostasis and protects podocytes against oxidative stress-induced injury both in vitro and in vivo. |Animals [MESH] |Apoptosis/*physiology [MESH] |Disease Models, Animal [MESH] |Kidney Glomerulus/metabolism/pathology [MESH] |Membrane Proteins/*metabolism [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Mitochondria/*metabolism/pathology [MESH] |Nephritis/*metabolism/pathology [MESH] |Oxidative Stress/*physiology [MESH] |Podocytes/*metabolism/pathology [MESH] |Proteinuria/metabolism/pathology [MESH]Mpv17 in mitochondria protects podocytes against mitochondrial dysfunc(epmc).pdf DeepDyve Pubget Overpricing