Transcriptomic profile of trametinib on LPS-mediated gene expression in murine peritoneal macrophages
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ABSTRACT: To determine the underlying mechanisms by which trametinib affected LPS-induced inflammatory response in macrophages, we performed microarrays to define the global gene expression in murine peritoneal macrophages treating with trametinib or vehicle followed by LPS stimulation.
Project description:Mouse peritoneal macrophages were isolated and treated with vehicle or C498 (15 μM) for 0.5 h, followed by LPS (100 ng/ml) challenge for an additional 4 h.
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:Here we study the effect of LPS in the transcriptome of thioglycollate-elicited peritoneal macrophages isolated from Ldlr knock out mice
Project description:We have identified a number of miRNAs that are differentially expressed in LPS treated mouse peritoneal macrophages, as compared to untreated cells
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: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.
Project description:Here we study the effect of LPS in the transcriptome of thioglycollate-elicited peritoneal macrophages isolated from Ldlr knock out and Ch25h;Ldlr double knock out mice
Project description:Setdb1 is one of the H3K9 methyltransferases and represses gene expression by H3K9 methylation. In an attempt to elucidate the role of Setdb1 in the TLR4-mediated inflammatory responses, we performed DNA microarray analysis using lipid A (the active component of LPS)-stimulated peritoneal macrophages from macrophage specific Setdb1 KO (KO) and WT mice. The genes upregulated by lipid A treatment in WT macrophages and further increased in KO macrophages contain many genes associated with interleukins and chemokines. Peritoneal macrophages from WT and KO mice were stimulated with lipid A 10 ng/ml or vehicle for 4 h. Microarray analysis was performed using Affymetrix Mouse 430 2.0.