Fxr-deficiency in mouse liver slices aggravates cyclosporin A toxicity by upregulation of pro-inflammatory genes and downregulation of genes involved in mitochondrial functions

Dataset

Description

The transcription factor farnesoid X receptor (FXR) governs bile acid and energy homeostasis, is involved in inflammation, and has protective functions in the liver. In the present study we investigated the effect of Fxr deficiency in mouse precision cut liver slices (PCLS) exposed to a model hepatotoxicant cyclosporin A (CsA). It was anticipated that Fxr deficiency could aggravate toxicity of CsA in PCLS and pinpoint to novel genes/processes regulated by FXR.
Date made available22 Oct 2015
PublisherRIKILT Wageningen UR

Research Output

Open Access
  • 4 Citations (Scopus)

    Cite this

    Szalowska, E. (Creator), Pronk, T. (Creator), Peijnenburg, A. (Creator) (22 Oct 2015). Fxr-deficiency in mouse liver slices aggravates cyclosporin A toxicity by upregulation of pro-inflammatory genes and downregulation of genes involved in mitochondrial functions. RIKILT Wageningen UR.