Effect of exogenous FABP4 (A-FABP/aP2) with and without palmitic acid on gene expression in RAW264.7 macrophages
Ontology highlight
ABSTRACT: Gene expression profile of FABP4 treatment in RAW264.7 macrophages was examined to show a ligand (palmitic acid)-dependent and a ligand-independent effect of FABP4. RAW264.7 macrophages were treated with and without 200 nM recombinant FABP4 in the absence and presence of 0.2 mM palmitic acid.
Project description:Gene expression profile of FABP4 treatment in RAW264.7 macrophages was examined to show a ligand (palmitic acid)-dependent and a ligand-independent effect of FABP4.
Project description:Gene expression profile of treatment with FABP4 or FABP5 in ADSC and 233A cells was examined. ADSC or 233A cells were treated with and without 1 µM recombinant FABP4 or FABP5.
Project description:Brucella, a notorious intracellular pathogen, causes chronic infections in many mammals, including humans. The twin-arginine translocation (Tat) pathway transports folded proteins across the cytoplasmic membrane; protein substrates translocated by Brucella include ABC transporters, oxidoreductases, and cell envelope biosynthesis proteins. Previously, we showed that a Tat mutant of Brucella melitensis M28 exhibits reduced survival within murine macrophages. In this study, we compared the host responses elicited by wild-type M28 and its Tat-mutant strains ex vivo. We utilized label-free quantitative proteomics to assess proteomic changes in RAW264.7 macrophages after infection with M28 and its Tat mutants.
Project description:The goal of the experiment was to demonstrate if the overexpression of human-Prune-1 in Triple Negative breast cancer cells induces M2-polarization of macrophages in vitro. For this purpose, murine primary cells from breast tumor developed by Genetically Engineered Mouse Models (GEMMs) of TNBC (i.e., MMTV-Wnt1) and metastatic TNBC overexpressing both human Prune-1 and Wnt1 in mammary gland (i.e., MMTV-Prune-1/Wnt1) were obtained. Conditioned media were collected from these primary cells (1x106 cells) after 24 hours. Murine macrophages (J774A.1 and Raw264.7; 1x106) were starved for six hours and then grown for 48 hours in those conditioned media collected from MMTV-Wnt1 and MMTV-Prune-1/Wnt1 cells. Untreated macrophages were used as negative control for the experiment.
Project description:A variety of genes are responsible for regulating osteoclastogenesis in response to RANK Ligand. Microarray analysis was used to identify genes sensitive to RANKL-induced osteoclastogenesis in RAW264.7 cells. RAW264.7 cells were incubated with 50 ng/mL RANKL or vehicle control (3 replicates each). After 48 h, total RNA were harvested by an RNeasy Plus Mini Kit (QIAGEN).
Project description:RAW264.7 macrophages infected with MNV-1 and mock infected gene expression measured by microarray. To be published in Waugh, E. Chen, A. Baird, M. Fleming, S. Brown, C.M. and V K. Ward (2014) Characterization of the chemokine response of RAW264.7 cells to infection by murine norovirus. Virus Genes Four Samples, two mock and two MNV-1 infected.
Project description:Toxoplasma strains are known to inhibit the expression of several interferon-gamma induced genes, and a type II strain was shown to dysregulate genome-wide responses to interferon-gamma in human fibroblasts (Kim et al., 2007, J Immunol.). In this study we aimed to determine the effect of infection with three clonal lineages of Toxoplasma, type I, II, and III strains on genome-wide interferon-gamma induced transcription in murine macrophages. We also assessed the effect of the two main Toxoplasma modulators of mouse macrophage transcription, ROP16 and GRA15 (Jensen et al., 2011, Cell Host Microbe). We used Affymetrix microarrays to analyze host cell transcription after Toxoplasma infection and interferon-gamma stimulation. RAW264.7 murine macrophages were left uninfected or infected with type I (RH), type I ?rop16 (RH ?rop16), type II (Pru), type II ?gra15 (Pru ?gra15), or type II (CEP) parasites at an MOI ~5 for 18 hours and subsequently stimulated with murine IFN-? for six hours. Plaque assays were done to assess parasite viability. Total RNA was isolated and hybridized to Affymetrix Mouse 430A 2.0 gene chips.
Project description:Mouse RAW264.7 macrophages were treated with LPS, IFNb, poly(rI:rC), poly(dA:dT), VSV, HSV, Sendai virus. Genes identified by Human Innate Immunity Interactome for type I Interferon (HI5) were examined for expression. qPCR gene expression profiling. RAW264.7 macrophages were used and treated separately as indicated in the summary. Equal amount total RNA from each group was used for gene expression analysis.
Project description:Microarray analysis determined that 7.82% (244/3334) of Brucella abortus genes were up-regulated and 5.4% (180/3334) were down-regulated in RAW264.7 macrophages, compared to free-living bacteria in TSB In the study, Brucela abortus was isolated from infected macrophages at 24 post-infection, DNA microarray was used to analysis the differentially expressed genes between intracellular bacteria and free-living ones in TSB
Project description:The advances in chemical proteomics have significantly expanded our understanding of the diversity and abundance of fatty-acylated proteins in eukaryotes, and reveal novel functions for these lipid protein modifications. Nonetheless, quantitative comparative proteomic analysis of fatty-acylated proteins in different cellular states is still challenging. To address these limitations, we systematically evaluated different proteomic methods (alk-16 chemical reporter and acyl-RAC) and established robust conditions to selectively and quantitatively profile fatty-acylated proteins in mammalian cells. Using a combination of metabolic labeling with fatty acid chemical reporters, selective chemical enrichment and label-free proteomics, we performed a quantitative analysis of fatty-acylated proteins in naïve and activated macrophages. These studies revealed novel fatty-acylated proteins associated with host immunity that are differently expressed and lipid-modified in different cellular states.