Effect of ApoE deficiency on microRNA expression in bone marrow derived macrophages (BMDM)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA996506 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25338387.fastq.gz | Fastqsanger.gz | |||
| SRR25338388.fastq.gz | Fastqsanger.gz | |||
| SRR25338389.fastq.gz | Fastqsanger.gz | |||
| SRR25338390.fastq.gz | Fastqsanger.gz | |||
| SRR25338391.fastq.gz | Fastqsanger.gz |
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Project description:ApoE exerts pleiotropic properties in controlling inflammation and myeloid cell activation. We here uncover microRNA regulation as yet another mechanism that ApoE acts upon to control immune cell activity and inflammatory response. We compared the expression of microRNAs in BMDM derived from ApoE-KO (EKO) or WIldtype (WT) mice and identified 78 microRNAs to be differentially expressed between these two groups. Among these microRNAs, we identified miR-146a-5p to be highly upregulated in WT BMDM as compared to EKO BMDM. This is consistent with our prior study that reports a role of ApoE in promoting the biogenesis of this microRNA via the transcription of its host gene PU.1 (Spi1) in monocytes/macrophages. Of note, miR-146a-5p is recognized as a potent inhibitor of the NF-κB signaling pathway via the inactivation of IRAK1 and TRAF6. Furthermore, we identified mIR-142a-3p as downregulated in WT BMDM as compared to EKO BMDM. This microRNA has been reported to control important metabolic functions in myeloid cells by targeting the long chain fatty acid transporter CPT1A, thereby inhibiting fatty acid oxidation. Our data thus uncovers another novel of ApoE in controlling lipid metabolism in myeloid cells by suppressing the expression of miR-142a-3p. Taken together, our data provide a novel framework for the microRNA signatures regulated by ApoE in myeloid cells. Moreover, we uncovered an important mechanism of which ApoE can regulate myeloid cell immunometabolism via the regulation of miR-146a-5p and miR-142a-3p.
2023-08-23 | GSE237727 | GEO
Project description:While ApoE expression by myeloid cells is recognized to control inflammation, whether such benefits can be communicated via extracellular vesicles including exosomes is not known. Through the study of exosomes produced by macrophages derived from the bone marrow of Wildtype (WT-BMDM-exo) and ApoE deficient (EKO-BMDM-exo) mice, we uncover a critical role of ApoE in regulating cell signaling properties. We treated splenic CD4+ T cells with EKO-BMDM-exo, WT-BMDM-exo, or PBS and performed gene expression profiling analysis. We found that CD4+ T cells treated with EKO-BMDM-exo show elevations in genes involved in the T-cell receptor complex (Cd3e, Cd247, & Cd4) and Il2rg, a key component of cytokine receptors on CD4+ T cells. Taken together, our data unveil a novel property of macrophage ApoE in controlling adaptive immunity by their secreted exosomes.
2023-08-23 | GSE237731 | GEO
Project description:While ApoE expression by myeloid cells is recognized to control inflammation, whether such benefits can be communicated via extracellular vesicles including exosomes is not known. Through the study of exosomes produced by macrophages derived from the bone marrow of Wildtype (WT-BMDM-exo) and ApoE deficient (EKO-BMDM-exo) mice, we uncover a critical role of ApoE in regulating cell signaling properties. We treated BMDM with EKO-BMDM-exo, WT-BMDM-exo, or PBS and performed gene expression profiling analysis. We found that BMDM treated with EKO-BMDM-exo show reductions in the cholesterol efflux gene Abca1 and the long chain fatty acid transporter Cpt1a. Furthermore, BMDM treated with EKO-BMDM-exo show reduced expressions of genes involved in oxidative stress response, particularly the glutathione peroxidases (Gpx1 & Gpx3) and the selenoproteins (Selenow, Selenom, Selenop, and Selenon). In contrast, treatments of these EKO-BMDM-exo upregulated the expressions of genes reported to drive glycolysis or involved in the glycolytic pathway (Aldh2, Pkm, Cd9, Fth1, Dio2, and Pgd). Taken together, our data unveil a novel property of macrophage ApoE in controlling the immunometabolism-regulatory properties by their secreted exosomes.
2024-07-18 | GSE237730 | GEO
Project description:Expression data from mouse bone marrow derived macrophages (BMDM)
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Project description:Microarray analysis of mouse bone marrow-derived macrophages (BMDM)
| PRJNA511464 | ENA
Project description:Investigation of whole genome gene expression level changes in BMDM adhered for 4 or 18hrs to Lab Tek Chamber slides pre-coated with 4ug/ml of human serum albumin (HSA) (control protein) or purified human C1q and treated with lipopolysaccharide (LPS: 20ng/ml) Mycobacterium avium 101 (M avium) or apoptotic Jurkat T cells. BMDM were obtained from C57Bl/6 and generated as previously described in Bohlson, SS, Strasser, JA, Bower JJ, Schorey J S 2001 Role of complement in Mycobacterium avium pathogenesis: in vivo and in vitro analyses of the host response to infection in the absence of complement component C3 Infec Immun 69: 7729-7735. Mybacterium avium 101 was obtained from Dr Jeff Schorey (University of Notre Dame). The human Jurkat T cell line was obtained from ATCC (Manassas, VA) and induced to undergo apoptosis with dexamethasone as described in Lillis, AP, Greenlee, M C, Mikhailenko I, Pizzo, S V, Tenner, A J, Strickland, D K, Bohlson, S S 2008 Murine Low-Density Lipoprotein Receptor-Related Protein 1 (LRP) Is Required for Phagocytosis of Targets Bearing LRP Ligands but Is Not Required for C1q-triggered Enhancement of Phagocytosis J Immunol 181: 364: 373. A six chip study using total RNA from 5 separate cultures of BMDM adhered to HSA for 4 hrs, 5 separate cultures of BMDM adhered to C1q for 4 hrs, 5 separate cultures of BMDM adhered to HSA for 4 hrs and infected with M avium at a 1:500 ratio of BMDM to M avium, 5 separate cultures of BMDM adhered to C1q for 4hrs and infected with M avium at a 1:500 ratio ofBMDM to M avium, 5 separate cultures of BMDM adhered to HSA for 4 hrs and infected with M avium at a 1:1000 ratio of BMDM to M avium, 5 separate cultures of BMDM adhered to HSA for 4 hrs and treated with 20ng/ml LPS, 5 separate cultures of BMDM adhered to C1q for 4 hrs and treated with 20ng/ml LPS, 5 separate cultures of BMDM adhered to HSA for 4 hrs and treated with 20ng/ml LPS and co-cultured with apoptotic Jurkat cells at a 1:3 ratio of BMDM to apoptotic cells, 5 separate cultures of BMDM adhered to C1q for 4 hrs and treated with 20ng/ml LPS and co-cultured with apoptotic Jurkat cells at a 1:3 ratio of BMDM to apoptotic cells, 5 separate cultures of BMDM adhered to HSA for 18 hrs, 5 separate cultures of BMDM adhered to C1q for 18 hrs, 5 separate cultures of BMDM adhered to HSA for 18 hrs and infected with M avium at a 1:500 ratio of BMDM to M avium, 5 separate cultures of BMDM adhered to C1q for 18hrs and infected with M avium at a 1:500 ratio of BMDM to M avium, 5 separate cultures of BMDM adhered to HSA for 18 hrs and infected with M avium at a 1:1000 ratio of BMDM to M avium. The chip utilized for these studies is a mouse whole-genome 12-plex expression microarray design by NimbleGen designed from the MM9 genome Candidate probe sequences were verified to have no cross-hybridization to human (HG19) or Mycobacterium avium (NC_008595) targets Note: Study sample BMDM_HSA & M avium (1:500)_18hr_rep2 was not included in this submission due to quality control concerns.
2012-03-01 | E-GEOD-35280 | biostudies-arrayexpress
Project description:Bone marrow cells were isolated, primed with M-CSF (M-BMDM) or GM-CSF (GM-BMDM) and cultured for 7 days. The proteomic difference between GM-BMDM and M-BMDM were analyzed to describe the phenotye and function of two types of macrophages.
2023-03-29 | PXD041180 |
Project description:Due to their ligand profiles, it can be hypothesized that Stab1 and Stab2 may be involved in atherosclerosis. We treated bone marrow derived macrophages (BMDM) with plasma from Stabilin-deficient and Wildtype mice to account for gene changes. We used microarrays to detail the global programme of gene expression in BMDM during different plasma treatments. We identified distinct classes of up- and down-regulated genes in response to the treatment.
2022-06-01 | GSE143533 | GEO
Project description:We analyzed global genome-wide transcriptional response of bone marrow derived macrophages (BMDM) to tunicamycin (TM). This analysis demonstrated that TM treatment changed the expression of 1,426 genes in WT BMDM and 1,075 genes in 4KO BMDM ( Casp1-/-Casp8-/-Casp11-/-Ripk3-/- ) (2-fold cut-off, p<0.05). Among differentially-expressed genes, all downregulated 759 genes were downregulated to similar levels in both WT and 4KO BMDM after TM treatment. However, 667 genes activated by TM treatment were globally upregulated to significantly higher levels in WT, compared to 4KO BMDM which is consistent with previous findings of a muted macrophage responses to triggers in cells lacking CASP8. Next we used gene set enrichment analysis to annotate pathways deregulated by TM in BMDM and compared down-regulated and upregulated gene sets in BMDM to their expression in liver resident Mf, Kupffer cells, at homeostatic conditions in vivo. The most prominently down-regulated pathways in BMDM after TM treatment were cell cycle, DNA replication, and metabolism pathways (normalized enrichment score (NES) =-8.5, -7.9, -7.1, respectively, FDR<1e-4,). Importantly, the gene sets constituting downregulated pathways in TM-treated BMDM were highly expressed in KC in vivo at homeostatic levels (NES= 8.7, 10.5, 6.6 , FDR<1e-4), suggesting the lack of phenotypic similarity between TM-treated BMDM and KC for this set of pathways. However, this same analysis showed that the most prominently enriched pathways in BMDM after TM treatment were pathways related to innate and adaptive immune signaling, cytokine signaling and mitogen-activated protein kinase signaling (NES =8.7, 6.4, 6.9, 3.2, respectively , FDR<1e-4). The gene set enrichment analysis for this set of genes demonstrated that in KC at homeostatic conditions, these same genes are also highly enriched (NES=12.6, 9.8, 7.1, 4.5 , FDR<1e-4), suggesting that for upregulated gene sets, TM treatment drives BMDM in vitro to transcriptomic phenotype similar to that observed in KC in vivo at homeostatic conditions.
2022-01-25 | GSE117042 | GEO
Project description:Chromatin from wild-type and NFAT5-deficient BMDM was immunoprecipitated with anti-NFAT5 antibodies and ultrasequenced to identify NFAT5 binding sites in steady state macrophages (BMDM)
2018-09-26 | GSE107948 | GEO