MRNA profile of Ch25h null ECs which were treated with PBS or mouse colorectal tumor extracellular vesicles in vitro.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE163941 | GEO | 2021/05/19
REPOSITORIES: GEO
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Project description:mRNA profile of Ch25h null ECs which were treated with PBS or mouse colorectal tumor extracellular vesicles in vitro.
| PRJNA688291 | ENA
Project description:Cholesterol 25-hydroxylase (Ch25h) has been previously demonstrated to be required for anti-inflammatory effect and anti-viral activity, while also promoting foam cell formation. In order to delineate the role of Ch25h in atherosclerosis, we isolated peritoneal macrophages (PMs) from mice lacking ApoE and Ch25h (i.e., ApoE-/-/Ch25h-/-) compared to their wildtype littermates (i.e., ApoE-/-/Ch25h+/+) for transcriptome analysis, in biological duplicates (n=12 pooled mice per group). Deep-sequencing analysis revealed that PMs ablated with Ch25h were prone to the pro-inflammatory M1 phenotype as well as increased cholesterol biosynthesis. Overall, we found that Ch25h is integral to atheroprotection through the preservation of M2 polarization and suppression of intracelllular cholesterol content.
2017-10-05 | GSE90983 | GEO
Project description:Microarray analysis of triplicate RNA samples isolated from kdrl:eGFP-sorted ECs of wildtype, npas4l-/-, etsrp-/-, and sox32-/- zebrafish embryos in Tg(kdrl:EGFP) transgenic background between 18 and 18.5 hpf.
2020-10-20 | E-MTAB-9698 | biostudies-arrayexpress
Project description:25-hydroxycholesterol has been demonstrated to regulate SREBP processing, yet Ch25h-deficient mice have no cholesterol abnormalities. Using RNA-seq, we find that LPS-stimulated, Ch25h-deficient BMDMs have dysregulated SREBP target genes, demonstrating that 25-hydroxycholesterol is an induced repressor of SREBP during inflammatory settings. mRNA profiles from day 7 M-CSF bone marrow-derived macrophages (wild type, Ch25h-knockout, LXR-double knockout, were generated by deep sequencing on an Illumina HiSeq 2500. Sequence reads passing a quality filter were aligned to the mouse genome (mm10) using STAR.
2014-08-08 | E-GEOD-58993 | biostudies-arrayexpress
Project description:The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis. However, the impact of endothelial-derived factors on other aspects of CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream Cholesterol-25-hydroxylase (Ch25h) promote neuroinflammation but their functions in the CNS remain unclear. Using a floxed-reporter Ch25h knock-in mice, we traced Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrated that Ch25h-specific ablation in ECs attenuates experimental autoimmune encephalomyelitis. Mechanistically, inflamed Ch25h-deficient CNS ECs displayed altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) expansion relative to other leukocyte subsets that suppress encephalitogenic T lymphocytes proliferation. Finally, endothelial Ch25h-deficiency combined with mobilization of immature neutrophils into circulation resulted in nearly complete EAE protection. Our findings reveal a central role for CNS endothelial-derived Ch25h in promoting neuroinflammation by regulating expansion of immunosuppressive myeloid cell populations.
2023-01-23 | GSE217431 | GEO
Project description:In this study we mutated the ecsAB operon in two different Staphylococcus aureus strains, Newman and LS-1, and performed a wide characterization of phenotypic effects of the mutations. A growth defect, increased autolysis and lysostaphin sensitivity, decreased levels of cell wall proteins and altered cell surface texture indicate that Ecs deficiency causes significant changes in the cell wall. The precursor form of staphylokinase was released into the wall in an Ecs-dependent manner. Pathogenicity of the ecs mutants was studied with a mouse arthritis model. Mice inoculated with ecs mutants developed markedly milder infections than when inoculated with the wild-type strains, as was illustrated by a lower mortality, less weight loss, decreased persistence of staphylococci in the kidneys and a milder arthritis. DNA microarray analysis revealed that inactivation of Ecs in S. aureus Newman caused either up-regulation or down-regulation of genes encoding various membrane transport proteins, particularly ABC transporters and phosphate-specific transport (PST) systems. Differentially expressed were also several genes encoding proteins involved in virulence, including the virulence factor regulator protein Rot, protein A, adhesins and capsular polysaccharide biosynthesis proteins. Furthermore, the susceptibility of ecs mutant to ribosomal antibiotics as well as the chelerythrine and sanguinarine plant alkaloids was increased. WT and ecsA mutant strains were hybridized at 3 and 6 hours of growth in rich medium (4-replicates)
2011-01-01 | E-GEOD-22353 | biostudies-arrayexpress
Project description:25-hydroxycholesterol has been demonstrated to regulate SREBP processing, yet Ch25h-deficient mice have no cholesterol abnormalities. Using RNA-seq, we find that LPS-stimulated, Ch25h-deficient BMDMs have dysregulated SREBP target genes, demonstrating that 25-hydroxycholesterol is an induced repressor of SREBP during inflammatory settings.
2014-08-08 | GSE58993 | GEO
Project description:Here we study the effect of LPS in the transcriptome of thioglycollate-elicited peritoneal macrophages isolated from Ldlr knock out and Ch25h;Ldlr double knock out mice
2022-07-01 | GSE189079 | GEO
Project description:Ecs is an ATP-binding cassette (ABC) transporter present in aerobic and facultative anaerobic gram-positive Firmicutes. Inactivation of Bacillus subtilis Ecs causes pleiotropic changes in the bacterial phenotype including inhibition of intramembrane proteolysis. The molecule(s) transported by Ecs is (are) still unknown. In this study we mutated the ecsAB operon in two Staphylococcus aureus strains, Newman and LS-1. Phenotypic and functional characterization of these Ecs deficient mutants revealed a defect in growth, increased autolysis and lysostaphin sensitivity, altered composition of cell wall proteins including the precursor form of staphylokinase and an altered bacterial surface texture. DNA microarray analysis indicated that the Ecs deficiency changed expression of the virulence factor regulator protein Rot accompanied by differential expression of membrane transport proteins, particularly ABC transporters and phosphate-specific transport systems, protein A, adhesins and capsular polysaccharide biosynthesis proteins. Virulence of the ecs mutants was studied in a mouse model of hematogenous S. aureus infection. Mice inoculated with the ecs mutant strains developed markedly milder infections than those inoculated with the wild-type strains and had consequently lower mortality, less weight loss, milder arthritis and decreased persistence of staphylococci in the kidneys. The ecs mutants had higher susceptibility to ribosomal antibiotics and plant alkaloids chelerythrine and sanguinarine. Our results show that Ecs is essential for staphylococcal virulence and antimicrobial resistance probably since the transport function of Ecs is essential for the normal structure and function of the cell wall. Thus targeting Ecs may be a new approach in combating staphylococcal infection.
2011-01-01 | GSE22353 | GEO