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

GSE63457

Mus musculus

20 Downloadable Samples

Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Submitter Supplied Information

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.

PubMed ID

26482353

Publication Title

Cyclosporin A induced toxicity in mouse liver slices is only slightly aggravated by Fxr-deficiency and co-occurs with upregulation of pro-inflammatory genes and downregulation of genes involved in mitochondrial functions.

Total Samples

Submitter’s Institution

RIKILT-Wageningen UR

Authors

Szalowska E, Pronk TE, Peijnenburg AA

Source Repository

Gene Expression Omnibus (GEO)

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