Project description:Purpose: To compare transcriptomic changes between untreated and LPS or CpG treated groups in WT, Lum-/- and Bgn-/- peritoneal macrophages.
Project description:Transcription profiling by array of LysMCre/Cre and KLF2/ (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with lipopolysaccharide (LPS) for 6 hours
Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).
Project description:We have identified a number of miRNAs that are differentially expressed in LPS treated mouse peritoneal macrophages, as compared to untreated cells Peritoneal macrophages treated with LPS for 0, 4, 12, 24h. RNA was isolated and miRNA array assays were performed by Exiqon (miRCURY™ LNA Array version 10.0)
Project description:Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation.
Project description:Analysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions. Total RNA obtained from isolated peritoneal macrophages isolated from DUSP3-/- and WT mice 36 hours after challenging them in vivo with PBS or with 6mg/kg of LPS.
Project description:Purpose: The cholinergic anti-inflammatory pathway (CAP) links the nervous and immune systems and modulates innate and adaptive immunity. The goals of this study are to identify the new downstream signaling of α7nAChR in macrophages. Methods: Peritoneal macrophages isolated from α7nAChR+/+ and α7nAChR-/- mice were treated with nicotine (10 μM) and/or LPS (100 ng/ml), then RNA-seq was performed. Results: Genes were selected that had more than 4-fold relative gene expression in nicotine-treated cells compared to the control group (vehicle-treated). The same calculation was applied to nicotine+LPS-treated cells and LPS-treated cells and 264 genes were identified as genes commonly induced by nicotine based on these two comparisons. Then relative gene expression was compared between α7nAChR+/+- and α7nAChR-/- -derived cells. 18 genes were finally selected whose expressions are suppressed (<1/2) in α7nAChR-/- -derived peritoneal macrophages. Conclusions: Our study represents the first detailed analysis focused on the new downstream signaling of α7nAChR in macrophages, generated by RNA-seq technology. We newly revealed the important anti-inflammatory role of Hes1 in the CAP using some functional experiments.
