Mus musculus
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ABSTRACT:
PROVIDER: PRJNA375115 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional and accessible chromatin profiles during conversion process of alternatively activated macrophages
| PRJNA375110 | ENA
Project description:Transcriptional and accessible chromatin profiles during conversion process of alternatively activated macrophages (ATAC-Seq)
| PRJNA375114 | ENA
Project description:Whether inflammatory macrophages can adopt features of the tissue resident niche and what mechanisms mediate phenotypic conversion remain unclear. In this study, we show by cell surface phenotyping, as well as by RNA-Seq transcriptional profiling and ATAC-Seq open chromatin regions profiling, that inflammatory monocyte can adopt a tissue resident phenotype, which is also accompanied by re-programming of the transcriptional profiles and remodeling of the open chromatin landscape. The conversion process is dependent on Vitamin A, suggesting that Vitamin A deficiency may lead to the failure to resolve inflammation, as inflammatory macrophages accumulate without adopting a tissue residency phenotype.
2017-04-24 | GSE95001 | GEO
Project description:Whether inflammatory macrophages can adopt features of the tissue resident niche and what mechanisms mediate phenotypic conversion remain unclear. In this study, we show by cell surface phenotyping, as well as by RNA-Seq transcriptional profiling and ATAC-Seq open chromatin regions profiling, that inflammatory monocyte can adopt a tissue resident phenotype, which is also accompanied by re-programming of the transcriptional profiles and remodeling of the open chromatin landscape. The conversion process is dependent on Vitamin A, suggesting that Vitamin A deficiency may lead to the failure to resolve inflammation, as inflammatory macrophages accumulate without adopting a tissue residency phenotype.
2017-04-24 | GSE95002 | GEO
Project description:Macrophage activation must be tightly controlled to prevent overzealous responses that cause self-damage. MicroRNAs have been shown to promote classical macrophage activation by blocking concomitant anti-inflammatory signals and transcription factors, but can also place restraints on activation by preventing excessive TLR-signalling. In contrast, the microRNA profile associated with alternatively activated macrophages and their role in regulating wound-healing or anti-helminthic responses has not yet been described. Utilizing an in vivo model of alternative activation, in which adult Brugia malayi nematodes are surgically implanted in the peritoneal cavity of mice, we examined the profile of microRNA expression in these alternatively activated macrophages and compared this to alternatively activated IL-4 receptor knockout macrophages and thioglycollate elicited macrophages. Peritoneal macrophages from BALB/c wild type or IL-4 receptor knockout mice were elicited with thioglycollate or using nemtodes (peritoneal implant of Brugia malayi). The latter leads to a population of alternatively activated macrophages. Microarray analysis was used to examine the microRNA profile of WT alternatively activated macrophages (n = 4), IL-4 receptor knockout alternatively activated macrophages (n = 4), WT thioglycollate elicited macrophages (n = 3) and IL-4 receptor knockout thioglycollate elicited macrophages (n = 3).
2012-08-07 | E-GEOD-35047 | biostudies-arrayexpress
Project description:Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue. Keywords: metabolic state analysis
2008-04-29 | GSE11295 | GEO
Project description:Expression data from human alternatively activated macrophages
| PRJNA122839 | ENA
Project description:A potent Th1 immune response is critical to the control of tuberculosis. The impact of an additive Th2 response on the course of disease has so far been insufficiently characterized, despite increased morbidity after coinfection with Mycobacterium tuberculosis and Th2 eliciting helminths and possible involvement of Th2 polarization in reactivation of latent tuberculosis. Here, we describe the gene expression profile of murine bone marrow derived macrophages alternatively activated by IL-4 to infection with M. tuberculosis. Comparison of transcriptional profiles of infected IL-4 and IFN-g activated macrophages revealed delayed and partially diminished responses in alternatively activated macrophages, characterized by reduced exposure to nitrosative stress and increased iron availability, respectively, to intracellular bacteria. Alternative activation of host macrophages correlated with elevated expression of the M. tuberculosis iron storage protein bfrB as well as reduced expression of the mycobactin synthesis genes mbtI and mbtJ. The extracellular matrix remodelling enzyme matrix metalloproteinase-12 (MMP-12) was induced in alternatively activated macrophages in vitro, and MMP-12 expressing macrophages were abundant at late, but not early, stages of tuberculosis in murine lungs. Our findings emphasize that alternative activation deprives macrophages of control mechanisms which limit mycobacterial growth in vivo, thus supporting intracellular persistence of M. tuberculosis. Keywords: transcriptome, gene regulation, macrophages, IL-4, IFN-gamma, nitric oxide
2006-01-01 | GSE3552 | GEO
Project description:Interleukin-4 (IL-4) activates macrophages to adopt a distinct phenotype important for tissue repair and helminth infection, but the molecular basis of chromatin remodeling in response to IL-4 stimulation is not understood. We find that IL-4 activation of terminally differentiated macrophages in mice is accompanied by cell-type-specific chromatin remodeling in regions enriched with binding motifs of the pioneer transcription factor PU.1. Mutation studies based on natural genetic variation between C57BL/6 and BALB/c mouse strains demonstrate that accessibility of these IL-4 induced regions can be regulated through differences in DNA shape, without disruption of pioneer factor motifs. We propose a model whereby DNA shape features of stimulation-dependent genomic elements contribute to differences in the accessible chromatin landscape of alternatively activated macrophages on different genetic backgrounds.
2020-01-04 | GSE116107 | GEO