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10.1681/ASN.2016070744

http://scihub22266oqcxt.onion/10.1681/ASN.2016070744
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C5407728!5407728!27895157
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suck abstract from ncbi


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pmid27895157      J+Am+Soc+Nephrol 2017 ; 28 (5): 1421-36
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  • Beneficial Effects of Myo-Inositol Oxygenase Deficiency in Cisplatin-Induced AKI #MMPMID27895157
  • Dutta RK; Kondeti VK; Sharma I; Chandel NS; Quaggin SE; Kanwar YS
  • J Am Soc Nephrol 2017[May]; 28 (5): 1421-36 PMID27895157show ga
  • Overexpression of the proximal tubular enzyme myo-inositol oxygenase (MIOX) induces oxidant stress in vitro. However, the relevance of MIOX to tubular pathobiology remains enigmatic. To investigate the role of MIOX in cisplatin-induced tubular AKI, we generated conditional MIOX-overexpressing transgenic (MIOX-TG) mice and MIOX-knockout (MIOX?/?) mice with tubule-specific MIOX overexpression or knockout, respectively. Compared with cisplatin-treated wild-type (WT) mice, cisplatin-treated MIOX-TG mice had even greater increases in urea, creatinine, and KIM-1 levels and more tubular injury and apoptosis, but these effects were attenuated in cisplatin-treated MIOX?/? mice. Similarly, MIOX-TG mice had the highest and MIOX?/? mice had the lowest renal levels of Bax, cleaved caspase-3, and NADPH oxidase-4 expression and reactive oxygen species (ROS) generation after cisplatin treatment. In vitro, cisplatin dose-dependently increased ROS generation in LLC-PK1 cells. Furthermore, MIOX overexpression in these cells accentuated cisplatin-induced ROS generation and perturbations in the ratio of GSH to oxidized GSH, whereas MIOX-siRNA or N-acetyl cysteine treatment attenuated these effects. Additionally, the cisplatin-induced enhancement of p53 activation, NF-?B binding to DNA, and NF-?B nuclear translocation in WT mice was exacerbated in MIOX-TG mice but absent in MIOX?/? mice. In vitro, MIOX-siRNA or NAC treatment reduced the dose-dependent increase in p53 expression induced by cisplatin. We also observed a remarkable influx of inflammatory cells and upregulation of cytokines in kidneys of cisplatin-treated MIOX-TG mice. Finally, analysis of genomic DNA in WT mice revealed cisplatin-induced hypomethylation of the MIOX promoter. These data suggest that MIOX overexpression exacerbates, whereas MIOX gene disruption protects against, cisplatin-induced AKI.
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