scholarly journals Investigating the role of nuclear receptors liver x receptor and retinoid x receptor in cartilage development and homeostasis

2017 ◽  
Vol 25 ◽  
pp. S147
Author(s):  
M.-G. Sun ◽  
A. Ratneswaran ◽  
H. Dupuis ◽  
F. Beier
Keyword(s):  
Nuclear Receptors ◽  
Liver X Receptor ◽  
Retinoid X Receptor ◽  
Cartilage Development

scholarly journals The role of nuclear receptors liver X receptor and retinoid X receptor in murine cartilage

2016 ◽  
Vol 24 ◽  
pp. S153-S154
Author(s):  
M.-G. Sun ◽  
A. Ratneswaran ◽  
H. Dupuis ◽  
F. Beier
Keyword(s):  
Nuclear Receptors ◽  
Liver X Receptor ◽  
Retinoid X Receptor

scholarly journals Investigating the role of Retinoid X Receptor in cartilage development and homeostasis

2019 ◽  
Vol 27 ◽  
pp. S177-S178
Author(s):  
M.-G. Sun ◽  
H. Dupuis ◽  
M. Miranda Rodrigues ◽  
L. Vi ◽  
F. Beier
Keyword(s):  
Retinoid X Receptor ◽  
Cartilage Development

scholarly journals Regulation of Macrophage Inflammatory Gene Expression by the Orphan Nuclear Receptor Nur77

2006 ◽  
Vol 20 (4) ◽  
pp. 786-794 ◽  
Author(s):  
Liming Pei ◽  
Antonio Castrillo ◽  
Peter Tontonoz
Keyword(s):  
Gene Expression ◽  
Nuclear Receptors ◽  
Transcriptional Activation ◽  
Liver X Receptor ◽  
Nuclear Hormone Receptor ◽  
Orphan Nuclear Receptor ◽  
Orphan Nuclear Receptors ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Abstract Members of the nuclear hormone receptor superfamily have emerged as important regulators of macrophage gene expression in inflammation and disease. Previous studies have shown that the lipid-activated receptors peroxisomal proliferator-activated receptor and liver X receptor inhibit nuclear factor-κB (NF-κB) signaling and inflammatory gene expression. We recently identified the NR4A subfamily of orphan nuclear receptors (Nur77/NR4A1, Nurr1/NR4A2, and NOR1/NR4A3) as lipopolysaccharide- and NF-κB-responsive genes in macrophages. However, the role of these transcription factors in macrophage gene expression is unknown. We demonstrate here that, in contrast to peroxisomal proliferator-activated receptor and liver X receptor, the role of NR4A receptors in macrophages is proinflammatory. Retroviral expression of Nur77 in macrophages leads to the transcriptional activation of multiple genes involved in inflammation, apoptosis, and cell cycle control. One particularly interesting Nur77-responsive gene is the inducible kinase IKKi/IKKε, an important component of the NF-κB signaling pathway. The IKKi promoter contains a functional NR4A binding site and is activated by all three NR4A receptors in transient transfection assays. Consistent with the activation of IKKi, expression of Nur77 in macrophages potentiates the induction of inflammatory gene expression in response to lipopolysaccharide. These results identify a new role for NR4A orphan nuclear receptors in the control of macrophage gene expression during inflammation.

scholarly journals Investigating the role of Retinoid X Receptor in cartilage development and homeostasis

2018 ◽  
Vol 26 ◽  
pp. S98 ◽  
Author(s):  
M.-G. Sun ◽  
A. Ratneswaran ◽  
H. Dupuis ◽  
F. Beier
Keyword(s):  
Retinoid X Receptor ◽  
Cartilage Development

Role of nuclear receptors and hepatocyte-enriched transcription factors for Ntcp repression in biliary obstruction in mouse liver

2005 ◽  
Vol 289 (5) ◽  
pp. G798-G805 ◽  
Author(s):  
Gernot Zollner ◽  
Martin Wagner ◽  
Peter Fickert ◽  
Andreas Geier ◽  
Andrea Fuchsbichler ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Bile Acid ◽  
Dna Binding ◽  
Nuclear Receptors ◽  
Farnesoid X Receptor ◽  
Acid Uptake ◽  
Mrna Levels ◽  
Uptake System ◽  
Duct Ligation

Expression of the main hepatic bile acid uptake system, the Na+-taurocholate cotransporter (Ntcp), is downregulated during cholestasis. Bile acid-induced, farnesoid X receptor (FXR)-mediated induction of the nuclear repressor short heterodimer partner (SHP) has been proposed as a key mechanism reducing Ntcp expression. However, the role of FXR and SHP or other nuclear receptors and hepatocyte-enriched transcription factors in mediating Ntcp repression in obstructive cholestasis is unclear. FXR knockout (FXR−/−) and wild-type (FXR+/+) mice were subjected to common bile duct ligation (CBDL). Cholic acid (CA)-fed and LPS-treated FXR−/− and FXR+/+ mice were studied for comparison. mRNA levels of Ntcp and SHP and nuclear protein levels of hepatocyte nuclear factor (HNF)-1α, HNF-3β, HNF-4α, retinoid X receptor (RXR)-α, and retinoic acid receptor (RAR)-α and their DNA binding were assessed. Hepatic cytokine mRNA levels were also measured. CBDL and CA led to Ntcp repression in FXR+/+, but not FXR−/−, mice, whereas LPS reduced Ntcp expression in both genotypes. CBDL and LPS but not CA induced cytokine expression and reduced levels of HNF-1α, HNF-3β, HNF-4α, RXRα, and RARα to similar extents in FXR+/+ and FXR−/−. DNA binding of these transactivators was unaffected by CA in FXR+/+ mice but was markedly reduced in FXR−/− mice. In conclusion, Ntcp repression by CBDL and CA is mediated by accumulating bile acids via FXR and does not depend on cytokines, whereas Ntcp repression by LPS is independent of FXR. Reduced levels of HNF-1α, RXRα, and RARα in CBDL FXR−/− mice and reduced DNA binding in CA-fed FXR−/− mice, despite unchanged Ntcp levels, indicate that these factors may have a minor role in regulation of mouse Ntcp during cholestasis.

The protective role of liver X receptor (LXR) during fumonisin B1-induced hepatotoxicity

2018 ◽  
Vol 93 (2) ◽  
pp. 505-517 ◽  
Author(s):  
Marion Régnier ◽  
Arnaud Polizzi ◽  
Céline Lukowicz ◽  
Sarra Smati ◽  
Frédéric Lasserre ◽  
...  
Keyword(s):  
Fumonisin B1 ◽  
Protective Role ◽  
Liver X Receptor

scholarly journals Activation of liver X receptor/retinoid X receptor pathway ameliorates liver disease inAtp7B−/−(Wilson disease) mice

Hepatology ◽  
2016 ◽  
Vol 63 (6) ◽  
pp. 1828-1841 ◽  
Author(s):  
James P. Hamilton ◽  
Lahari Koganti ◽  
Abigael Muchenditsi ◽  
Venkata S. Pendyala ◽  
David Huso ◽  
...  
Keyword(s):  
Liver Disease ◽  
Wilson Disease ◽  
Liver X Receptor ◽  
Retinoid X Receptor

scholarly journals Liver X Receptor regulates Th17 and RORγt+ Treg cells by distinct mechanisms

2019 ◽  
Author(s):  
Sara M. Parigi ◽  
Srustidhar Das ◽  
Annika Frede ◽  
Rebeca F. Cardoso ◽  
Kumar Parijat Tripathi ◽  
...  
Keyword(s):  
Lymph Node ◽  
Nuclear Receptors ◽  
Th17 Cells ◽  
Immune Modulation ◽  
Treg Cells ◽  
Liver X Receptor ◽  
Commensal Bacteria ◽  
T Helper ◽  
Mesenteric Lymph ◽  
Th Cell

AbstractThe gastrointestinal microenvironment, dominated by dietary compounds and the commensal bacteria, is a major driver of intestinal CD4+ T helper (Th) cell differentiation. Dietary compounds can be sensed by nuclear receptors (NRs) that consequently exerts pleiotropic effects including immune modulation. However, how NRs regulate distinct intestinal Th subsets remain poorly understood. Here, we found that under homeostatic condition Liver X receptor (LXR), a sensor of cholesterol metabolites, controls RORγt+ Treg and Th17 cells in the intestine draining mesenteric lymph node (MLN). Mechanistically, while lack of LXR signaling in CD11c+ myeloid cells led to an increase in RORγt+ Treg, modulation of MLN Th17 was independent of LXR signaling in either immune or epithelial cells. Of note, LXRα modulated only the Th17 cells, but not RORγt+ Treg in the MLN and horizontal transfer of microbiota between LXRα−/− and WT mice was sufficient to partially increase the MLN Th17 in WT mice. While LXRα deficiency increased the abundance of Ruminococcaceae and Lachnospiraceae bacterial families compared to the WT littermates, microbiota ablation including ablation of SFB was not sufficient to dampen LXRα-mediated expansion of MLN Th17. Altogether, our results suggest that LXR modulates RORγt+ Treg and Th17 cells in the MLN through distinct mechanisms.

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