Mus musculus
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ABSTRACT:
PROVIDER: PRJNA148715 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MiR expression profile in M1-polarized bone marrow derived macrophage cells compared with normal mouse aortic tissue.
| PRJNA142283 | ENA
Project description:The global change of the miR expression profile during atherosclerosis is due to the infiltration of different types of leukocytes into the arterial vessel wall in addition to disease-specific regulation in vascular cells. Monocyte-derived macrophage accumulation in the subintimal region is critical in the formation of atherosclerotic plaques. It is currently unknown which miRs are involved in the atherogenic macrophage response. The comparison of the miR expression profile in LPS/Interferon-gamma activated mouse macrophages with the miR expression in the unstimulated mouse macrophages was performed to detect M1-type macrophage-enriched miRs. This screening combined with our miR profiling in atherosclerotic vessels may help to identify M1-type macrophage-enriched miRs in atherosclerotic vessels that may play a role in the macrophage function during atherogenesis. Bone marrow cells were harvested from femura of 6- to 8-week-old female C57BL/6 mice, re-suspended in DMEM-F12/10% FCS/10% L929-conditioned medium, and cultured for 7 days to differentiate into primary macrophages. F4/80 and CD11b expression was determined by flow cytometry to confirm the macrophage phenotype. Macrophages were stimulated with LPS (100ng/ml, 14 hours) and INF-g (10ng/ml, 6 hours), and the M1 polarization was verified by quantification of mannose receptor C type 1 (MRC1), arginase II (ArgII), inducible nitric oxide synthase (iNOS), and arginase I (ArgI) by qRT-PCR. Total RNA (M1-type and unstimulated (MФ) macrophages) was isolated using the mirVana microRNA Isolation Kit.
2012-12-26 | E-GEOD-33453 | biostudies-arrayexpress
Project description:Unstimulated (M0), M1-polarized (GM-CSF, LPS, IFNγ-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
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
Project description:Purpose: RNA-sequencing was performed to identify gene expression changes between bone marrow derived macrophages isolated from wildtype and mirn23a-/- (Mirc11-/-) mice that were either M1 or M2 polarized. Results: Diferential gene expression was examined between wildtype and mirn23a-/- M1 polarized macrophages and wildtype and mirn23a-/- M2 polarized macrophages. The number of genes with significant (p<0.05) 2-fold changes in our M1 dataset is 4-fold higher than the 2-fold changed genes in our M2 dataset. 43 unique genes were differentially expressed over 2-fold in M1 mutant macrophages compared to wildtype with 29 upregulated and 14 downregulated. 10 genes (8 downregulated/ 2 upregulated)were differentially expressed in mirn23a-/- M2 macrophages by at least 2-fold compared to wildtype.
2020-11-18 | GSE159762 | GEO
Project description:We report the gene expression (obtained by next generation RNAseq) of bone marrow derived macrophages from Lyz2Cre+ or C57Bl/6 mice that have been polarized to an M1 or M2 phenotype in the presence of absence of EGFR inhibitor, Erlotinib. This study provides data on how M1 and M2 BMDMs differ in their overall gene expression profiles in mice as well as how gene expression is influenced by EGFR inhibition during polarization.
2021-03-02 | GSE167982 | GEO
Project description:Classically activated (M1) macrophages protect from infection but can cause inflammatory disease and tissue damage while alternatively activated (M2) macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. The inflammation-associated miRNA, miR-155, was rapidly up-regulated over 100-fold in M1, but not M2, macrophages. Inflammatory M1 genes and proteins iNOS, IL-1b and TNF-a were reduced up to 72% in miR-155 knockout mouse macrophages, but miR-155 deficiency did not affect expression of genes associated with M2 macrophages (e.g., Arginase-1). Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed iNOS and TNF-a gene expression in wild-type M1 macrophages. Comparative transcriptional profiling of unactivated (M0) and M1 macrophages derived from wild-type and miR-155 knockout (KO) mice revealed an M1 signature of approximately 1300 genes, half of which were dependent on miR-155. Real-Time PCR of independent datasets validated miR-155's contribution to induction of iNOS, IL-1b, TNF-a, IL-6 and IL-12, as well as suppression of miR-155 targets Inpp5d, Tspan14, Ptprj and Mafb. Overall, these data indicate that miR-155 plays an essential role in driving the differentiation and effector potential of inflammatory M1 macrophages. Total RNA was prepared from bone marrow-derived macrophages of miR-155 knockout mice (n=2 independent mice) treated in M0, M1 or M2 conditions (n=2 replicates per condition originating from different mice)
2016-07-15 | E-GEOD-77425 | biostudies-arrayexpress
Project description:The global change of the miR expression profile during atherosclerosis is due to the infiltration of different types of leukocytes into the arterial vessel wall in addition to disease-specific regulation in vascular cells. Monocyte-derived macrophage accumulation in the subintimal region is critical in the formation of atherosclerotic plaques. It is currently unknown which miRs are involved in the atherogenic macrophage response. The comparison of the miR expression profile in LPS/Interferon-gamma activated mouse macrophages with the miR expression in the unstimulated mouse macrophages was performed to detect M1-type macrophage-enriched miRs. This screening combined with our miR profiling in atherosclerotic vessels may help to identify M1-type macrophage-enriched miRs in atherosclerotic vessels that may play a role in the macrophage function during atherogenesis.
2012-12-26 | GSE33453 | GEO
Project description:In order to determine P2X7R secretome we analyzed the proteins present in cell-free supernatants from wild-type (P2rx7+/+) or P2rx7-/- bone marrow-derived macrophages (BMDMs) polarized either to M1 or M2 and subsequently treated with ATP. BMDMs were primed with LPS (M1) or IL-4 (M2) for 4 hours and the proteins secreted during this step were extensively washed with PBS before ATP was added in fresh buffer. The complex mixture of proteins obtained in the macrophages supernatants after ATP stimulation were fractionated using one dimension gel electrophoresis and 10 bands were selected for LC-MS/MS analysis based in their presence in higher intensity in P2rx7+/+ supernatant compared with P2rx7-/- supernatant.
2016-03-11 | PXD001981 | Pride
Project description:Gene expression from WT and NFAT5 KO primary macrophage cultures. Keywords: Bone-marrow derived macrophages. We analyzed 4 arrays from each condition: unstimulated WT BMDMs, LPS stimulated WT BMDMs, unstimulated KO BMDMs, LPS stimulated KO BMDMs.
2012-01-20 | E-GEOD-26343 | biostudies-arrayexpress