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- W205152811 abstract "Our studies in a murine model of cecal ligation and puncture (CLP)-induced sepsis show that iNOS-derived reactive nitrogen species (RNS) generated by the tubular epithelium play a major role in acute kidney injury (AKI) associated with sepsis. Unfortunately, sepsis-induced AKI is a complex disease and difficult to model in vitro. To address the need to study the mechanism of tubular oxidant generation and injury, we developed a new, more relevant in vitro model where mIMCD-3 (murine tubular epithelial cells) are treated with media containing 5% serum collected from mice at 4h after induction of sepsis (CLP) or Sham (no sepsis). After exposure to Sham or CLP serum, induction of iNOS (by RT-PCR) occurred and NO generation increased at 6h by 83% (P < .05 compared to Sham). This was accompanied by a 74% or 72% increase in RNS measured by oxidation of carboxy-H2DCFDA or dihydrorhodamine 123, respectively, and a 30% increase in cytotoxicity (lactate dehydrogenase release) in cells treated with CLP serum (P < .05 compared to Sham). To analyze the source of the oxidants and injury, mIMCD-3 cells were treated with iNOS inhibitor L-N6-(1-iminoethyl) lysine (L-NIL). L-NIL (1mM) completely blocked NO generation, RNS generation, and cytotoxicity (P < .05). Therefore, it appears this new cellular model is relevant for studying the mechanism of renal epithelial oxidant generation and injury induced by sepsis. Supported by NIH DK075991." @default.
- W205152811 created "2016-06-24" @default.
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- W205152811 date "2010-04-01" @default.
- W205152811 modified "2023-09-27" @default.
- W205152811 title "Reactive nitrogen species generation in a new in‐vitro model of sepsis‐induced renal epithelial injury" @default.
- W205152811 doi "https://doi.org/10.1096/fasebj.24.1_supplement.968.3" @default.
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