Regulation ot TAM gene expression by ABCA1 and ABCG1 (4 Cre- and 4 Cre+)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA520922 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression was analyzed in TAM from mice injected with ID8 ovarian cancer cells intraperitoneally in ABC a1/g1 fl/fl-LysM-Cre mice. Tumor-associated macrophages (TAM) have been shown to have important roles in the malignant progression of various cancers. However, macrophages also posses intrinsic tumoricidal activity and can promote the activity of cytotoxic lymphocytes, but they rapidly adopt an alternative phenotype within tumors, associated with immune-suppression and trophic functions that support tumor growth. The mechanisms that promote TAM polarization in the tumor-microenvironment remain poorly understood, these mechanisms may represent important therapeutic targets to block the tumor-promoting functions of TAM and restore their anti-tumor potential. Here we have characterized TAM in a mouse model of metastatic ovarian cancer. We show that ovarian cancer cells promote membrane-cholesterol efflux and the depletion of lipid rafts from macrophages. Increased cholesterol efflux promoted IL-4 mediated reprogramming while inhibiting IFNg-induced gene expression. These studies reveal an unexpected role for tumor-induced membrane-cholesterol efflux in driving the IL-4 signaling and the tumor-promoting functions of TAM, while rendering them refractory to pro-inflammatory stimuli. Thus, preventing cholesterol efflux in TAM could represent a novel therapeutic strategy to block pro-tumor functions and restore anti-tumor immunity.
2019-02-05 | GSE126079 | GEO
Project description:ATP binding cassette subfamily member 1 (ABCA1) and G1 (ABCG1) are cholesterol efflux transporter to prevent excess intracellular cholesterol accumulation. We here report the deletion of Abca1 and Abcg1 results in the significant increased expression of Cd38, a multi-faceted ectoenzyme with NADase activity.
2024-04-17 | GSE234507 | GEO
Project description:Cholesterol is the precursor of all steroids, but how cholesterol flux is controlled in steroidogenic tissues is poorly understood. The cholesterol exporter ABCG1 is an essential component of the reverse cholesterol pathway and its systemic inactivation results in neutral lipid redistribution to macrophages. However, the function of ABCG1 in steroidogenic organs is not explored. To model this question, we inactivated the ortholog Abcg1 gene in the mouse adrenal cortex. Abcg1 disruption led to an adrenal-specific increase in transcripts involved in cholesterol uptake and de novo synthesis, and to an 80% increase in corticosterone production. Importantly, this phenotype was not recapitulated by inactivation of the cholesterol exporter Abca1. The absence of any change in lipid profile suggested that adrenal Abcg1 is not involved in cholesterol export to a clinically relevant extent.
2023-09-05 | GSE242081 | GEO
Project description:Splenocytes were separated from Lrrc8af/f and Lrrc8af/f Cd4-Cre;OT-I mice. The splenocytes were stimulated with indicated peptides (unstime/ SIINFEKL-10pM(NL)/ SIINFEKL-1000pM(NH)/ SIIGFEKL-1000nM(G4)) for 6 hours. The OT-I CD8+ T cells were labeled with Va2-PE/CD8-A700 and sorted for the sequencing.
2023-09-26 | GSE243985 | GEO
Project description:Regulation ot TAM gene expression by Pi3K (WT vs p110d-/-)
| PRJNA520925 | ENA
Project description:Transcriptional profiling of cytokines and its receptors in lungs from 8 month old chow-fed wild-type and ABCG1-/- mice Keywords: genotype comparison; inflammatory mediators 4 individual mice per group; RNA from inferior left lobe; WT vs. ABCG1-/-
2010-05-25 | E-GEOD-8976 | biostudies-arrayexpress
Project description:Gene expression was analyzed in peritoneal macrophages and TAM from mice injected with ID8 ovarian cancer cells intraperitoneally 28 days after tumor implantation. Tumor-associated macrophages (TAM) have been shown to have important roles in the malignant progression of various cancers. However, macrophages also posses intrinsic tumoricidal activity and can promote the activity of cytotoxic lymphocytes, but they rapidly adopt an alternative phenotype within tumors, associated with immune-suppression and trophic functions that support tumor growth. The mechanisms that promote TAM polarization in the tumor-microenvironment remain poorly understood, these mechanisms may represent important therapeutic targets to block the tumor-promoting functions of TAM and restore their anti-tumor potential. Here we have characterized TAM in a mouse model of metastatic ovarian cancer. We show that ovarian cancer cells promote membrane-cholesterol efflux and the depletion of lipid rafts from macrophages. Increased cholesterol efflux promoted IL-4 mediated reprogramming while inhibiting IFNg-induced gene expression. These studies reveal an unexpected role for tumor-induced membrane-cholesterol efflux in driving the IL-4 signaling and the tumor-promoting functions of TAM, while rendering them refractory to pro-inflammatory stimuli. Thus, preventing cholesterol efflux in TAM could represent a novel therapeutic strategy to block pro-tumor functions and restore anti-tumor immunity.
2019-02-05 | GSE126080 | GEO
Project description:Effects of deletioin of cholesterol efflux genes Abca1 and Abcg1 on other gene expressions in macrophages
| PRJNA981554 | ENA
Project description:OT-I T cell activation in Lrrc8af/f and Lrrc8af/f Cd4-Cre OT-I mice
| PRJNA1020844 | ENA
Project description:Transcriptional profiling of cytokines and its receptors in lungs from 8 month old chow-fed wild-type and ABCG1-/- mice Keywords: genotype comparison; inflammatory mediators
2008-07-30 | GSE8976 | GEO