NFAT5 ChIP-seq in mouse bone marrow-derived macrophages (BMDM) [2016]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE107950 | GEO | 2018/09/26
REPOSITORIES: GEO
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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
Project description:NFAT5 ChIP-seq in mouse bone marrow-derived macrophages (BMDM) [2016]
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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:Bmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by cytokine stimulation total RNA was harvested at 2, 4, 6, 24 hrs Total RNA was collected from bmdm cells stimulated with IFNg at different time point
2015-04-30 | E-GEOD-59207 | biostudies-arrayexpress
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish danger signal induced inflammatory response. BMDM from C57/BL6 mice cultred in the presence or absence of heat shock necrotic A20 cells for 1hr. Control sample (Non_4) is 'BMDM in the absence of necrotic A20 cells' and reference sample (Dead_4) is 'BMDM in the presence of necrotic A20 cells'
2014-08-08 | E-GEOD-58003 | biostudies-arrayexpress
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:The aim of this study was to interrogate whether BMDM basal or pro-inflammatory stimulated gene expression is altered by diabetes and persists despite in vitro glucose normalisation. Unstimulated BMDM from diabetic mice differentially express 632 genes (324 increased and 308 downregulated) compared to unstimulated control BMDM; this increases to 1,348 genes (802 increased and 546 decreased) upon stimulation (FDR<0.05, FC>1.5).
2019-01-08 | GSE124774 | GEO
Project description:Oncogenic KRAS is now considered a druggable target; however, multiple mechanisms contribute to the development of resistance to KRAS-targeted therapy. A significant factor in therapy resistance is the alteration in cell state or cellular plasticity, exemplified by the epithelial-to-mesenchymal transition (EMT) phenotype. In pancreatic ductal adenocarcinoma (PDAC), the negative correlation between addiction to oncogenic KRAS signaling and EMT has been observed, yet the role of cell plasticity and its underlying mechanisms in governing resistance remain unclear. Our findings reveal that the pivotal EMT driver, TGFβ, facilitates KRAS bypass in PDAC through the nuclear factor NFAT5. NFAT5 interacts with canonical TGFβ factors SMAD3 and SMAD4, inducing EMT and therapy resistance. To identify DNA bound by the NFAT5-SMADs complex, we conducted Chromatin IP followed by next-generation sequencing (ChIP-seq) using antibodies binding to NFAT5, SMAD2, SMAD3, and SMAD4.
2024-10-09 | GSE252838 | GEO