Transcriptomic analysis of kidney cortex following the KLF6 induction
Ontology highlight
ABSTRACT: The goal of this study was to identify transcriptomic changes mediated by KLF6 induction in the setting of STZ-induced diabetic kidney disease
Project description:The goal of this study was to identify genome-wide chromatin accessibility changes caused by podocyte specific overexpression of KLF6 in STZ + UNX induced diabetic mouse model.
Project description:The goal of this study was to identify transcriptomic changes mediated by KLF6 induction 24 hours after aristolochic acid-induced acute kidney injury
Project description:The goal of this study was to identify chromatin changes mediated by KLF6 induction 24 hours after aristolochic acid-induced acute kidney injury
Project description:identified cluster of microRNAs significantly increased in kidney glomeruli from diabetic mice compared to nondiabetic control mice RNAs from kidney glomeruli from control mice and STZ-injected diabetic mice were extracted.
Project description:Altered cellular metabolism in kidney proximal tubule (PT) cells plays a critical role in the development and progression of acute kidney injury (AKI). The transcription factor Krüppel-like factor 6 (KLF6) is rapidly and robustly induced in the PT after AKI, suggesting an early-inducible injury response gene. PT-specific Klf6 knockdown (Klf6PTKO) are protected from AKI and resulting fibrosis in mice. Combined RNA-sequencing and ChIP-sequencing demonstrated preserved expression of genes encoding branched chain amino acid (BCAA) catabolic enzymes in Klf6PTKO mice, with several of the genes also having KLF6 binding sites close to their transcription start sites. Conversely, inducible KLF6 overexpression suppressed expression of BCAA genes and exacerbated kidney injury and fibrosis in mice. Injured kidney cells could not respond to the BCAA catabolic activator BT2, and injured cells overexpressing KLF6 were less able to utilize BCAA. Thus, targeting KLF6-mediated suppression of BCAA catabolism may serve as key therapeutic target in AKI and kidney fibrosis.