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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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MiRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

ABSTRACT: MicroRNAs regulated by lipopolysaccharide (LPS) target genes that contribute to the inflammatory phenotype. Here we showed that the protein kinase Akt1, which is activated by LPS, positively regulated miRNAs let-7e, miR-181c but negatively regulated miR-155 and miR-125b. In silico analyses and transfection studies revealed that let-7e repressed Toll-like receptor 4 (TLR4) whereas miR-155 repressed SOCS1, two proteins critical for LPS-driven TLR signalling, which regulate endotoxin sensitivity and tolerance. As a result, Akt1-/- macrophages exhibited increased responsiveness to LPS in culture and Akt1-/- mice did not develop endotoxin tolerance in vivo. Overexpression of let-7e and suppression of miR-155 in Akt1-/- macrophages restored sensitivity and tolerance to LPS in culture and in animals. These results indicate that Akt1 regulates the response of macrophages to LPS by controlling miRNA expression. The data deposited here contain the entire analysis of miRNA profile of Akt1+/+ and Akt1-/- thioglycollate elicited peritoneal macrophages following stimulation with LPS for 3 hours in culture. Thioglycollate elicited macrophages were cultured in complete DMEM medium, stimulated with LPS for 3 hours and RNA was extracted. Samples were analyzed using Taq-man PCR miRNA arrays (Dana Farber microarray Facility).

ORGANISM(S): Mus musculus

SUBMITTER: Christos Tsatsanis

PROVIDER: E-GEOD-17421 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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miRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

Project description:MicroRNAs regulated by lipopolysaccharide (LPS) target genes that contribute to the inflammatory phenotype. Here we showed that the protein kinase Akt1, which is activated by LPS, positively regulated miRNAs let-7e, miR-181c but negatively regulated miR-155 and miR-125b. In silico analyses and transfection studies revealed that let-7e repressed Toll-like receptor 4 (TLR4) whereas miR-155 repressed SOCS1, two proteins critical for LPS-driven TLR signalling, which regulate endotoxin sensitivity and tolerance. As a result, Akt1-/- macrophages exhibited increased responsiveness to LPS in culture and Akt1-/- mice did not develop endotoxin tolerance in vivo. Overexpression of let-7e and suppression of miR-155 in Akt1-/- macrophages restored sensitivity and tolerance to LPS in culture and in animals. These results indicate that Akt1 regulates the response of macrophages to LPS by controlling miRNA expression. The data deposited here contain the entire analysis of miRNA profile of Akt1+/+ and Akt1-/- thioglycollate elicited peritoneal macrophages following stimulation with LPS for 3 hours in culture.

2009-08-21 | GSE17421 | GEO

Morphine induced sepsis is mediated by abrogation of endotoxin tolerance through modulation of miR-146a, but not miR-155.

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Morphine induced sepsis is mediated by abrogation of endotoxin tolerance through modulation of miR-146a, but not miR-155.

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Project description:miRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

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Genome-wide gene expression analysis during endotoxin tolerance in PBMCs.

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LPS Tolerance inhibits cellular respiration and induces global changes in the secretome

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The activation of inflammatory response genes by LPS is blocked by HDAC inhibitor Trichostatin A (TSA)

Project description:TSA treatment blocks LPS-induction of several inflammatory target genes in primary macrophages. The microarray experiment was performed to identify LPS-inducible, LXR-sensitive target genes that retained LPS-induction in the presence of TSA. Thioglycollate-elicited macrophages were isolated from mice by peritoneal lavage 3 days following peritoneal injection of 2.5 ml 3% thioglycollate (DIFCO). Cells were plated in RPMI medium 1640 and 10% fetal bovine serum, washed after 5 h the medium was removed and cells were fed with fresh medium containing 0.5% fetal bovine serum. Cells were treated with TSA (Wako) at 100nM and/or with LPS (Sigma) at concentration of 100 ng/ml in the absence or presence of receptor-specific agonist for LXR (GW3965) at 1 µM. Keywords: TSA, LPS, LXR agonist

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