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10.1152/ajprenal.00485.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00485.2015 C4773829!4773829!26739891     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 310 (5): F409-15 Nephropedia Template TP {{tp|p=26739891|t=2016. Knockdown of RTN1A attenuates ER stress and kidney injury in albumin overload-induced nephropathy |pdf=|usr=}}{{26739891}} gab.com Text Knockdown of RTN1A attenuates ER stress and kidney injury in albumin overload-induced nephropathy JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26739891 #FOAvip Our previous studies have suggested a critical role of reticulon (RTN)1A in mediating endoplasmic reticulum (ER) stress in kidney cells of animal models and humans with kidney diseases. A large body of evidence suggests that proteinuria itself can cause tubular cell injury leading to the progression of kidney disease. In the present study, we determined whether RTN1A mediates proteinuria-induced tubular cell injury through increased ER stress. We found that incubation of HK2 cells with human serum albumin induced the expression of RTN1A and ER stress markers, whereas knockdown of RTN1A expression attenuated human serum albumin-induced ER stress and tubular cell apoptosis in vitro. In vivo, we found that tubular cell-specific RTN1 knockdown resulted in a significant attenuation of tubular cell ER stress, apoptosis, and renal fibrosis in a model of albumin overload nephropathy. Based on these findings, we conclude that RTN1A is a key mediator for proteinuria-induced tubular cell toxicity and renal fibrosis. Twit Text FOAVip Knockdown of RTN1A attenuates ER stress and kidney injury in albumin overload-induced nephropathy ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26739891 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26739891 #FOAvip English Wikipedia <ref>{{Cite pmid|26739891}}</ref> Knockdown of RTN1A attenuates ER stress and kidney injury in albumin overload-induced nephropathy #MMPMID26739891 Xiao W; Fan Y; Wang N; Chuang PY; Lee K; He JC Am J Physiol Renal Physiol 2016[Mar]; 310 (5): F409-15 PMID26739891show ga Our previous studies have suggested a critical role of reticulon (RTN)1A in mediating endoplasmic reticulum (ER) stress in kidney cells of animal models and humans with kidney diseases. A large body of evidence suggests that proteinuria itself can cause tubular cell injury leading to the progression of kidney disease. In the present study, we determined whether RTN1A mediates proteinuria-induced tubular cell injury through increased ER stress. We found that incubation of HK2 cells with human serum albumin induced the expression of RTN1A and ER stress markers, whereas knockdown of RTN1A expression attenuated human serum albumin-induced ER stress and tubular cell apoptosis in vitro. In vivo, we found that tubular cell-specific RTN1 knockdown resulted in a significant attenuation of tubular cell ER stress, apoptosis, and renal fibrosis in a model of albumin overload nephropathy. Based on these findings, we conclude that RTN1A is a key mediator for proteinuria-induced tubular cell toxicity and renal fibrosis. äKnockdown of RTN1A attenuates ER stress and kidney injury in albumin o(epmc).pdf DeepDyve Pubget Overpricing