Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription

Introduction: Macrophages abundantly express liver X receptors (LXRs), which are ligand-dependent transcription factors and sensors of several cholesterol metabolites. In response to agonists, LXRs promote the expression of key lipid homeostasis regulators. Cross talk between LXRs and inf...

Full description

Saved in:
Bibliographic Details
Main Authors: Estibaliz Glaría, Pol Rodríguez Martínez, Joan Font-Díaz, Juan Vladimir De la Rosa, Antonio Castrillo, Dylan J. Crawshaw, Jose Manuel Vidal Taboada, Josep Saura, Jonathan Matalonga, Eduardo Nunes Chini, Carme Caelles, Annabel F. Valledor
Format: Article
Language:English
Published: Karger Publishers 2025-01-01
Series:Journal of Innate Immunity
Online Access:https://karger.com/article/doi/10.1159/000543274
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849321636022452224
author Estibaliz Glaría
Pol Rodríguez Martínez
Joan Font-Díaz
Juan Vladimir De la Rosa
Antonio Castrillo
Dylan J. Crawshaw
Jose Manuel Vidal Taboada
Josep Saura
Jonathan Matalonga
Eduardo Nunes Chini
Carme Caelles
Annabel F. Valledor
author_facet Estibaliz Glaría
Pol Rodríguez Martínez
Joan Font-Díaz
Juan Vladimir De la Rosa
Antonio Castrillo
Dylan J. Crawshaw
Jose Manuel Vidal Taboada
Josep Saura
Jonathan Matalonga
Eduardo Nunes Chini
Carme Caelles
Annabel F. Valledor
author_sort Estibaliz Glaría
collection DOAJ
description Introduction: Macrophages abundantly express liver X receptors (LXRs), which are ligand-dependent transcription factors and sensors of several cholesterol metabolites. In response to agonists, LXRs promote the expression of key lipid homeostasis regulators. Cross talk between LXRs and inflammatory signals exists in a cell type- and gene-specific manner. A common feature in the macrophage response to inflammatory mediators is the induction of CCAAT/enhancer-binding protein beta (C/EBPβ), a master transcriptional regulator and lineage-determining transcription factor in monocytes/macrophages. Methods: Quantitative real-time PCR in control and C/EBPβ-deficient macrophages was used to explore the role of C/EBPβ in the cross talk between inflammatory mediators and the macrophage response to pharmacological LXR activation. The functional interaction between C/EBPβ and LXRs on selected genomic regions was further characterized by chromatin-immunoprecipitation (ChIP) and gene reporter studies. Results: Whereas inflammatory signaling repressed several LXR-regulated genes involved in lipid metabolism, these effects were conserved after deletion of C/EBPβ. In contrast, inflammatory mediators and LXRs synergistically induced the expression of the multifunctional protein CD38 in a C/EBPβ-dependent manner. C/EBPβ and LXRs bound to several regions with enhancer activity upstream and within the mouse Cd38 gene and their functional cooperation in macrophages required intact binding sites for LXR and C/EBPβ. Conclusion: This study reveals positive cross talk between C/EBPβ and LXRs during the macrophage inflammatory response, which selectively impacts CD38 expression.
format Article
id doaj-art-c0d3cd2842e04e02a1e89b011f59e040
institution Kabale University
issn 1662-8128
language English
publishDate 2025-01-01
publisher Karger Publishers
record_format Article
series Journal of Innate Immunity
spelling doaj-art-c0d3cd2842e04e02a1e89b011f59e0402025-08-20T03:49:41ZengKarger PublishersJournal of Innate Immunity1662-81282025-01-01171567710.1159/000543274Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 TranscriptionEstibaliz GlaríaPol Rodríguez MartínezJoan Font-DíazJuan Vladimir De la RosaAntonio CastrilloDylan J. CrawshawJose Manuel Vidal TaboadaJosep SauraJonathan MatalongaEduardo Nunes ChiniCarme CaellesAnnabel F. Valledor Introduction: Macrophages abundantly express liver X receptors (LXRs), which are ligand-dependent transcription factors and sensors of several cholesterol metabolites. In response to agonists, LXRs promote the expression of key lipid homeostasis regulators. Cross talk between LXRs and inflammatory signals exists in a cell type- and gene-specific manner. A common feature in the macrophage response to inflammatory mediators is the induction of CCAAT/enhancer-binding protein beta (C/EBPβ), a master transcriptional regulator and lineage-determining transcription factor in monocytes/macrophages. Methods: Quantitative real-time PCR in control and C/EBPβ-deficient macrophages was used to explore the role of C/EBPβ in the cross talk between inflammatory mediators and the macrophage response to pharmacological LXR activation. The functional interaction between C/EBPβ and LXRs on selected genomic regions was further characterized by chromatin-immunoprecipitation (ChIP) and gene reporter studies. Results: Whereas inflammatory signaling repressed several LXR-regulated genes involved in lipid metabolism, these effects were conserved after deletion of C/EBPβ. In contrast, inflammatory mediators and LXRs synergistically induced the expression of the multifunctional protein CD38 in a C/EBPβ-dependent manner. C/EBPβ and LXRs bound to several regions with enhancer activity upstream and within the mouse Cd38 gene and their functional cooperation in macrophages required intact binding sites for LXR and C/EBPβ. Conclusion: This study reveals positive cross talk between C/EBPβ and LXRs during the macrophage inflammatory response, which selectively impacts CD38 expression.https://karger.com/article/doi/10.1159/000543274
spellingShingle Estibaliz Glaría
Pol Rodríguez Martínez
Joan Font-Díaz
Juan Vladimir De la Rosa
Antonio Castrillo
Dylan J. Crawshaw
Jose Manuel Vidal Taboada
Josep Saura
Jonathan Matalonga
Eduardo Nunes Chini
Carme Caelles
Annabel F. Valledor
Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription
Journal of Innate Immunity
title Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription
title_full Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription
title_fullStr Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription
title_full_unstemmed Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription
title_short Liver X Receptors and Inflammatory-Induced C/EBPβ Selectively Cooperate to Control CD38 Transcription
title_sort liver x receptors and inflammatory induced c ebpβ selectively cooperate to control cd38 transcription
url https://karger.com/article/doi/10.1159/000543274
work_keys_str_mv AT estibalizglaria liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT polrodriguezmartinez liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT joanfontdiaz liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT juanvladimirdelarosa liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT antoniocastrillo liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT dylanjcrawshaw liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT josemanuelvidaltaboada liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT josepsaura liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT jonathanmatalonga liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT eduardonuneschini liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT carmecaelles liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription
AT annabelfvalledor liverxreceptorsandinflammatoryinducedcebpbselectivelycooperatetocontrolcd38transcription