Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Volume 1812, Issue 8, August 2011, Pages 851-858
ReviewActivation of bile salt nuclear receptor FXR is repressed by pro-inflammatory cytokines activating NF-κB signaling in the intestine☆
Under an Elsevier user license
open archive
Research highlights
► TNFα decreases FXR target gene expression in differentiated HT29 intestinal cells. ► TNFα and IL-1β decrease ileal FXR target gene expression ex vivo in WT mice. ► In the DSS model of murine colitis, FXR target gene expression is decreased. ► TNFα, IL-1β and overexpression of NF-κB subunits P50/P65 decrease FXR transcriptional activity. ► Intestinal inflammation inhibits FXR activation, probably via NF-κB-dependent tethering of FXR.
Abbreviations
BDL
bile duct ligation
CD
Crohn disease
DSS
dextran sodium sulfate
EV
empty vector
FGF
fibroblast growth factor
FXR
farnesoid X receptor
GAPDH
glyceraldehyde 3-phosphate dehydrogenase
GST
glutathione S-transferase
IBABP
intestinal bile acid binding protein
IBD
inflammatory bowel disease
IL
interleukin
KO
knock-out
NF-κB
nuclear factor κappa B
NR
nuclear receptor
RXR
retinoid X receptor
SHP
small heterodimer partner
TNBS
trinitrobenzene sulphonic acid
TNFα
tumor necrosis factor alpha
UC
ulcerative colitis
WT
wild type
Keywords
Inflammatory bowel disease
Nuclear factor κB
Farnesoid X Receptor
Mutual inhibition
Cited by (0)
- ☆
This article is part of a Special Issue entitled: Translating nuclear receptors from health to disease.
- 1
These authors share last authorship.
Copyright © 2011 Elsevier B.V. All rights reserved.