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10.1093/toxsci/kfu130 http://scihub22266oqcxt.onion/10.1093/toxsci/kfu130 C4271126!4271126!24973089     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24973089&cmd=llinks): Failed to open stream: HTTP request failed! 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Loss of ?(E)-Catenin Potentiates Cisplatin-Induced Nephrotoxicity via Increasing Apoptosis in Renal Tubular Epithelial Cells |pdf=|usr=}}{{24973089}} gab.com Text Loss of (E)-Catenin Potentiates Cisplatin-Induced Nephrotoxicity via Increasing Apoptosis in Renal Tubular Epithelial Cells JO: Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=24973089 #FOAvip Cisplatin is one of the most potent and widely used antitumor drugs. However, the use of cisplatin is limited by its side effect, nephrotoxicity. Evidence has shown an increased incidence and severity of acute kidney injury (AKI) in the elderly. Previous studies from our laboratory demonstrate a decrease in ?(E)-catenin expression in aged kidney. In this study, we investigated whether the loss of ?(E)-catenin may increase cisplatin nephrotoxicity. To study the effects of reduced ?(E)-catenin, a cell line with stable knockdown of ?(E)-catenin (C2 cells) was used; NT3 is nontargeted control. C2 cells exhibited a significant loss of viability as determined by MTT assay compared with NT3 cells after cisplatin challenge, but showed no difference in lactate dehydrogenase (LDH) leakage. Increased caspase 3/7 activation and PARP cleavage was observed in C2 cells after cisplatin treatment. Z-VAD, a pan-caspase inhibitor, abolished the difference in susceptibility between NT3 and C2 cells. Interestingly, the expression of ?(E)-catenin was further decreased after cisplatin treatment. Furthermore, in vivo data demonstrated a significant increase in serum creatinine at 72 h after a single dose of cisplatin in 24-month-old rats, but not in 4-month-old rats. Increased expression of KIM-1 and in situ apoptosis were also detected in aged kidney after cisplatin challenge. Taken together, these data suggest that loss of ?(E)-catenin increases apoptosis of tubular epithelial cells which may contribute to the increased nephrotoxicity induced by cisplatin in aged kidney. Twit Text FOAVip Loss of (E)-Catenin Potentiates Cisplatin-Induced Nephrotoxicity via Increasing Apoptosis in Renal Tubular Epithelial Cells ????Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=24973089 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24973089 #FOAvip English Wikipedia <ref>{{Cite pmid|24973089}}</ref> Loss of ?(E)-Catenin Potentiates Cisplatin-Induced Nephrotoxicity via Increasing Apoptosis in Renal Tubular Epithelial Cells #MMPMID24973089 Wang X; Grunz-Borgmann EA; Parrish AR Toxicol Sci 2014[Sep]; 141 (1): 254-62 PMID24973089show ga Cisplatin is one of the most potent and widely used antitumor drugs. However, the use of cisplatin is limited by its side effect, nephrotoxicity. Evidence has shown an increased incidence and severity of acute kidney injury (AKI) in the elderly. Previous studies from our laboratory demonstrate a decrease in ?(E)-catenin expression in aged kidney. In this study, we investigated whether the loss of ?(E)-catenin may increase cisplatin nephrotoxicity. To study the effects of reduced ?(E)-catenin, a cell line with stable knockdown of ?(E)-catenin (C2 cells) was used; NT3 is nontargeted control. C2 cells exhibited a significant loss of viability as determined by MTT assay compared with NT3 cells after cisplatin challenge, but showed no difference in lactate dehydrogenase (LDH) leakage. Increased caspase 3/7 activation and PARP cleavage was observed in C2 cells after cisplatin treatment. Z-VAD, a pan-caspase inhibitor, abolished the difference in susceptibility between NT3 and C2 cells. Interestingly, the expression of ?(E)-catenin was further decreased after cisplatin treatment. Furthermore, in vivo data demonstrated a significant increase in serum creatinine at 72 h after a single dose of cisplatin in 24-month-old rats, but not in 4-month-old rats. Increased expression of KIM-1 and in situ apoptosis were also detected in aged kidney after cisplatin challenge. Taken together, these data suggest that loss of ?(E)-catenin increases apoptosis of tubular epithelial cells which may contribute to the increased nephrotoxicity induced by cisplatin in aged kidney. äLoss of ?(E)-Catenin Potentiates Cisplatin-Induced Nephrotoxicity via (epmc).pdf DeepDyve Pubget Overpricing