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MiRNA expression profiling of murine LPS-stimulated dendritic cells exposed to quercetin

ABSTRACT: miRNA expression profiling of murine LPS-stimulated dendritic cells exposed to quercetin

PROVIDER: PRJNA445691 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6897850.fastq.gz	Fastqsanger.gz
	SRR6897860.fastq.gz	Fastqsanger.gz
	SRR6897851.fastq.gz	Fastqsanger.gz
	SRR6897861.fastq.gz	Fastqsanger.gz
	SRR6897852.fastq.gz	Fastqsanger.gz

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miRNA expression profiling of murine LPS-stimulated dendritic cells exposed to quercetin

Project description:Dendritic cells (DCs) are the most potent antigen-presenting cells that play an important role in the crosstalk between the innate and the adaptive immune response. We identified quercetin exposure as an effective strategy to suppress DCs inflammatory response induced by LPS. In this study, using NGS analysis, we examined the effect of quercetin on miRNAs expression in DCs. We defined a signature of 113 miRNAs differentially regulated in LPS-stimulated DCs after quercetin exposure. Among them, we observed an upregulation of miR-369-3p that potentially regulated C/EBP-beta. We functionally demonstrate that the loss of function of miR-369-3p in LPS-stimulated DCs during quercetin exposure led to an increase of C/EBP-beta and its downstream targets TNFα and IL6. Conversely, we showed that the ectopic induction of miR-369-3p even without quercetin suppresses the inflammatory response of LPS reducing C/EBP-beta, TNFα and IL6 production. In vivo, oral administration of quercetin induces miR-369-3p expression. These data demonstrate that a key mediator of immunosuppressive effect of quercetin is miR-369-3p. These findings could have potentially therapeutic implications since the induction of miR-369-3p expression may have anti-inflammatory effect.

2019-12-31 | GSE112327 | GEO

Wild type and ATG5-KO mouse dendritic cells exposed to interleukin-4 (IL4) and/or lipopolisaccharyde (LPS)

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Project description:Interleukin-2 (IL-2) is one of the molecules produced by mouse dendritic cells (DCs) after stimulation by Toll like receptor (TLR) agonists. By analogy with the events following T-cell receptor (TCR) engagement leading to IL-2 production we have observed that DC stimulation with lipopolysaccharide (LPS) induces Src-family kinase and phospholipase C (PLC)Î³2 activation, influx of extracellular Ca2+ and calcineurin-dependent nuclear NFAT translocation. We have also observed that the initiation of this pathway is independent of TLR4 engagement, and dependent exclusively on CD14. To determine the role of NFAT in LPS activated dendritic cells we have performed microarray analysis in conditions allowing or inhibiting NFAT activation. We show here that LPS-induced NFAT activation via CD14 is necessary to cause death of terminally differentiated DCs, an event that is essential for maintaining self-tolerance and preventing autoimmunity. Consequently, blocking this pathway in vivo causes prolonged DC survival and an increase in T cell priming capability. Gene expression analyses were performed using Affymetrix GeneChips in the following groups of murine bone marrow-derived dendritic cells: 1) CD14-deficient BMDCs stimulated with LPS; 2) wtBMDCs stimulated with LPS in presence of EGTA; 3) wtBMDCs stimulated with LPS. This experimental setting allowed us to select for effects due to Ca2+ fluxes and exclude the effects due to other causes, particularly the block of TRIF recruitment in CD14-deficient cells and the EGTA effects unrelated to Ca2+ chelation.

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Project description:We cultured bone marrow derived dendritic cells from WT and CD11c KO mice. Then, a group of bone marrow dendritic cells were stimulated with LPS overnight. We obtained bone marrow derived dendritic cells with or without LPS stimulation and analyzed proteomics profiles.

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