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10.1371/journal.pone.0048952 http://scihub22266oqcxt.onion/10.1371/journal.pone.0048952 23145036!3493596!23145036     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2012 ; 7 (11): e48952 Nephropedia Template TP {{tp|p=23145036|t=2012. Hypoxia-inducible factor activation protects the kidney from gentamicin-induced acute injury |pdf=|usr=}}{{23145036}} gab.com Text Hypoxia-inducible factor activation protects the kidney from gentamicin-induced acute injury JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=23145036 #FOAvip Gentamicin nephrotoxicity is one of the most common causes of acute kidney injury (AKI). Hypoxia-inducible factor (HIF) is effective in protecting the kidney from ischemic and toxic injury. Increased expression of HIF-1alpha mRNA has been reported in rats with gentamicin-induced renal injury. We hypothesizd that we could study the role of HIF in gentamicin-induced AKI by modulating HIF activity. In this study, we investigated whether HIF activation had protective effects on gentamicin-induced renal tubule cell injury. Gentamicin-induced AKI was established in male Sprague-Dawley rats. Cobalt was continuously infused into the rats to activate HIF. HK-2 cells were pre-treated with cobalt or dimethyloxalylglycine (DMOG) to activate HIF and were then exposed to gentamicin. Cobalt or DMOG significantly increased HIF-1alpha expression in rat kidneys and HK-2 cells. In HK-2 cells, HIF inhibited gentamicin-induced reactive oxygen species (ROS) formation. HIF also protected these cells from apoptosis by reducing caspase-3 activity and the amount of cleaved caspase-3, and -9 proteins. Increased expression of HIF-1alpha reduced the number of gentamicin-induced apoptotic cells in rat kidneys and HK-2 cells. HIF activation improved the creatinine clearance and proteinuria in gentamicin-induced AKI. HIF activation also ameliorated the extent of histologic injury and reduced macrophage infiltration into the tubulointerstitium. In gentamicin-induced AKI, the activation of HIF by cobalt or DMOG attenuated renal dysfunction, proteinuria, and structural damage through a reduction of oxidative stress, inflammation, and apoptosis in renal tubular epithelial cells. Twit Text FOAVip Hypoxia-inducible factor activation protects the kidney from gentamicin-induced acute injury ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=23145036 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23145036 #FOAvip English Wikipedia <ref>{{Cite pmid|23145036}}</ref> Hypoxia-inducible factor activation protects the kidney from gentamicin-induced acute injury #MMPMID23145036 Ahn JM; You SJ; Lee YM; Oh SW; Ahn SY; Kim S; Chin HJ; Chae DW; Na KY PLoS One 2012[]; 7 (11): e48952 PMID23145036show ga Gentamicin nephrotoxicity is one of the most common causes of acute kidney injury (AKI). Hypoxia-inducible factor (HIF) is effective in protecting the kidney from ischemic and toxic injury. Increased expression of HIF-1alpha mRNA has been reported in rats with gentamicin-induced renal injury. We hypothesizd that we could study the role of HIF in gentamicin-induced AKI by modulating HIF activity. In this study, we investigated whether HIF activation had protective effects on gentamicin-induced renal tubule cell injury. Gentamicin-induced AKI was established in male Sprague-Dawley rats. Cobalt was continuously infused into the rats to activate HIF. HK-2 cells were pre-treated with cobalt or dimethyloxalylglycine (DMOG) to activate HIF and were then exposed to gentamicin. Cobalt or DMOG significantly increased HIF-1alpha expression in rat kidneys and HK-2 cells. In HK-2 cells, HIF inhibited gentamicin-induced reactive oxygen species (ROS) formation. HIF also protected these cells from apoptosis by reducing caspase-3 activity and the amount of cleaved caspase-3, and -9 proteins. Increased expression of HIF-1alpha reduced the number of gentamicin-induced apoptotic cells in rat kidneys and HK-2 cells. HIF activation improved the creatinine clearance and proteinuria in gentamicin-induced AKI. HIF activation also ameliorated the extent of histologic injury and reduced macrophage infiltration into the tubulointerstitium. In gentamicin-induced AKI, the activation of HIF by cobalt or DMOG attenuated renal dysfunction, proteinuria, and structural damage through a reduction of oxidative stress, inflammation, and apoptosis in renal tubular epithelial cells. |Acute Kidney Injury/*chemically induced/*metabolism[MESH] |Amino Acids, Dicarboxylic/pharmacology[MESH] |Animals[MESH] |Apoptosis/drug effects[MESH] |Caspase 3/metabolism[MESH] |Caspase 9/metabolism[MESH] |Cells, Cultured[MESH] |Cobalt/pharmacology[MESH] |Gentamicins/*toxicity[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism[MESH] |Inflammation/metabolism[MESH] |Kidney Tubules/*drug effects/*metabolism[MESH] |Male[MESH] |Oxidative Stress/drug effects[MESH] |Random Allocation[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH]Hypoxia-inducible factor activation protects the kidney from gentamici(epmc).pdf DeepDyve Pubget Overpricing