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• W2129956077 startingPage "F1107" @default.
• W2129956077 abstract "The degree of albuminuria is a well-known adverse prognostic indicator in human glomerular diseases. However, the mechanisms by which albuminuria by itself contributes to tubulointerstitial injury and progression of renal disease remain unclear. We tested the hypothesis that apoptosis may represent one of the mechanisms by which tubule epithelial cells are damaged after albumin overload in vitro. Cultured LLC-PK(1) proximal tubule cells were incubated with varying concentrations of BSA. This resulted in a dose- and duration-dependent induction of apoptosis, as evidenced by internucleosomal DNA cleavage (DNA laddering and nick-end labeling), externalization of plasma membrane phosphatidylserine (annexin labeling), and characteristic morphological changes (cell shrinkage and nuclear condensation). Albumin overload also resulted in a dose-dependent upregulation of Fas and Fas-associated protein with death domain (FADD), and activation of caspase 8. Incubation with the caspase 8 inhibitor IETD ameliorated the albumin-induced apoptosis. Collectively, our results indicate that albumin overload induces apoptosis of cultured LLC-PK(1) cells, mediated at least in part by the Fas-FADD-caspase 8 pathway." @default.
• W2129956077 created "2016-06-24" @default.
• W2129956077 creator A5023385682 @default.
• W2129956077 creator A5032730476 @default.
• W2129956077 creator A5067234338 @default.
• W2129956077 date "2001-06-01" @default.
• W2129956077 modified "2023-09-27" @default.
• W2129956077 title "Albumin overload induces apoptosis in LLC-PK₁cells" @default.
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• W2129956077 doi "https://doi.org/10.1152/ajprenal.2001.280.6.f1107" @default.
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