Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression analysis of microRNAs in INT-HA-induced M2-like macrophages and untreated macrophages (M0)

ABSTRACT: Using the highly sensitive miRNA microarray, we screened 107 up-regulated microRNAs and 33 down-regulated microRNAs in the INT-HA-induced M2-like macrophages and we explored the functions of these miRNAs in macrophage polarization. The enrichment results indicated that these miRNAs might participate in the process of macrophage polarization. Furthermore, the quantitative real-time polymerase chain reaction results showed that miR-935 may play an important role in M2 macrophage polarization which was activated by INT-HA.

ORGANISM(S): Merkel cell polyomavirus Betapolyomavirus hominis Human alphaherpesvirus 2 JC polyomavirus Human betaherpesvirus 6B Betapolyomavirus macacae Homo sapiens Human immunodeficiency virus 1 Herpesvirus saimiri (strain 11)

PROVIDER: GSE110339 | GEO | 2021/02/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression analysis of microRNAs in INT-HA-induced M2-like macrophages and untreated macrophages (M0)

Project description:Expression analysis of microRNAs in INT-HA-induced M2-like macrophages and untreated macrophages (M0)

| PRJNA433494 | ENA

Genome wide trimethyl-H3K27 distibution in macrophages from wild-type and Jmjd3-/- macrophages.

Project description:Jmjd3 is trimethyl H3K27 specific demethylase required for M2 macrophage polarization. Genomic fragments obtained from wild-type and Jmjd3-/- mouse macrophages were immunoprecipitated with anti H3K27me3 Ab, and deep sequencing was performed. wild-type and Jmjd3-/- macrophages

2010-08-22 | E-GEOD-23297 | biostudies-arrayexpress

Genome wide trimethyl-H3K27 distibution in macrophages from wild-type and Jmjd3-/- macrophages.

2010-08-22 | GSE23297 | GEO

Functional and Transcriptomic Characterization of iPSC-derived Macrophages and their Application in Modeling Mendelian Disease

Project description:Using RNA-Seq, we reported novel findings in the comparison of transcriptome profiles of isogenic HMDM and IPSDM during differentiation and polarization. First, IPSDM lost expression of pluripotency markers, had remarkably distinct gene expression profiles relative to precursor iPSCs, and had largely similar gene expression as HMDM. Second, macrophage polarization to M1 was associated with a dramatic change in the transcriptome; expression profiles of IPSDM- and HMDM-derived M1 lines were highly correlated with each other but much less so with their respective IPSDM and HMDM precursors. Third, M2-HMDM lines had limited difference in gene expression compared to their non-polarized precursors, likely due to the known M2-like phenotype of M-CSF differentiated macrophages and their similarity to the IL-4 derived M2 phenotype Finally, through RNA-Seq we identified many new genes modulated during polarization in both HMDM and IPSDM thus providing novel, and potentially regulatory, candidates that warrant further study. iPS, IPSDM (including M1/M2) and HMDM (including M1/M2)cells were sequenced by Illumina HiSeq 2000 with poly-A selection

2015-07-08 | E-GEOD-55536 | biostudies-arrayexpress

FoxO1 is a regulator of MHC-II expression and anti-tumor effect of tumor associated macrophages

Project description:Bone marrow derived macrophages from C57BL/6 mice were stimulated into M1 and M2 polarization state. Analysis of BMDMs from LysMcre;FoxO1Fl/FL mice and control littermates. Results provide insight into the regulatory role of FoxO1 during macrophage polarization. BMDMs were stimulated with 100ng/ml LPS plus 20ng/ml IFN-γ into M1 polarization, and stimulated with 10ng/ml IL-4 plus 10ng/ml IL-13 into M2 polarization. Both for 24 hours. Unstimulated cells as M0 state.

2018-09-01 | GSE97260 | GEO

Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice.

Project description:Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell–like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization. 15 samples; 2 genotypes and 2 time points

2012-03-22 | E-GEOD-36669 | biostudies-arrayexpress

The multifaceted responses of human monocytes to IFN-gamma and IL-4 are not reducible to M1/M2 polarization of Macrophages

Project description:Macrophages are known to be polarized into inflammatory (M1) and immunoregulatory (M2) cells when they are stimulated by agonists such as IFN-gamma and IL-4, respectively. If circulating monocytes may be polarized in response to T cell signals is often misguidedly deduced from macrophage results. Here the transcriptional responses of human CD14+ monocytes to IFN-gamma and IL-4 were analyzed using whole genome microarrays. A principal component analysis and hierarchical clustering showed that monocyte and macrophage responses were distinct. Monocytes stimulated with IFN-gamma and IL-4 for 6 hours exhibited some features of macrophage polarization. Indeed, when 80 genes considered as M1 and M2 genes were analyzed, we found that M1 genes were modulated in response to IFN-gamma and that M2 genes were modulated in response to IL-4. The M1 polarization of monocytes was transient because only M2 genes were modulated when monocytes were stimulated with IFN-gamma and IL-4 for 18 hours. However, the activation of monocytes by IFN-gamma and IL-4 could not be reduced to M1/M2 polarization status. Indeed, monocytes exhibited early specific signatures composed of 46 and 39 up-regulated genes in response to IFN-gamma and IL-4, respectively, and a late signature common to both molecules that consisted of 57 up-regulated genes. Taken together, these results demonstrated the extreme plasticity of human monocytes and suggested the existence of a core transcriptional termination program. Using early and late signatures might be pertinent to investigate monocyte activation in inflammatory or infectious diseases. Monocytes were stimulated with IFN-gamma (20ng/mL) or IL-4 (20ng/mL) for 6 and 18 hours or culture for 6 and 18 hours without agonist (Unstimulated samples). Monocytes-derived-macrophages (MDM) stimulated with IFN-gamma and IL-4 for 18 hours were used as controls. Each microarray is derived from a single biological sample.

2013-03-15 | E-GEOD-36537 | biostudies-arrayexpress

Novel transcriptome signatures and markers defining murine macrophages at the extremes of the canonical M1 and M2 polarization spectrum

Project description:Classically (M1) and alternatively activated (M2) macrophages play distinct roles in various physiological and disease processes. Understanding the gene transcription programs that contribute to macrophage polarization along the M1/M2 spectrum may lead to new tools to detect and therapeutically manipulate macrophage phenotype. Here, we define the M1 and M2 macrophage signature through mRNA microarray. The M1 macrophage signature was defined by 629 up-regulated and 732 down-regulated genes while the M2 macrophage signature was formed by 388 up-regulated and 425 down-regulated genes. While a subset of probes was common to both M1 and M2 cells, others were exclusive to each macrophage subset. The common M1/M2 pathways were characterized by changes in various transcriptional regulators and signaling partners, including increases in Kruppel-like Factor (Klf) 4, but decreases in Klf2. To identify M1 and M2 biomarkers that help discriminate these populations, we selected genes that were increased during M1 or M2 differentiation but decreased in the opposite population. Among top novel M1-distinct genes, we identified CD38, G-protein coupled receptor 18 (Gpr18) and Formyl peptide receptor 2 (Fpr2). Among top M2 genes, we found early growth response protein 2 (Egr2) and Myc. We validated these genes by Real-Time PCR and developed a CD38/Egr2-based flow cytometry assay that discriminates between M1 and M2 macrophages. Overall, this work defines the M1 and M2 signature and identifies several novel M1 and M2 genes that may be used to distinguish and manipulate M1 and M2 macrophages. Total RNA was prepared from bone marrow-derived macrophages of wild-type mice (n=2-3 independent mice) treated in M0, M1 or M2 conditions (n=2-3 replicates per condition originating from different mice)

2015-12-08 | E-GEOD-69607 | biostudies-arrayexpress

Tissue transglutaminase exacerbates renal fibrosis via alternative activation of monocyte-derived macrophages

Project description:To elucidate the reason why the tissue transglutaminase (TG2) knockdown and inactivation suppressed M2 macrophage polarization, we explored genes whose expression was regulated by TG2 activity and investigated the molecular mechanism underlying this.

2023-03-03 | GSE222284 | GEO

Microarray of non-polarized and M1- and M2-polarized canine macrophages in vitro

Project description:Unstimulated (M0), M1-polarized (GM-CSF, LPS, IFNÎ³-stimulated), and M2-polarized (M-CSF, IL-4-stimulated) canine blood-derived macrophages were generated in vitro and investigated for differences in their transcriptome to create a basis for future investigations upon the role of macrophage polarization in dogs, a species, which has emerging importance for translational research.

2017-08-10 | E-MTAB-5458 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data