Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

ABSTRACT: Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

PROVIDER: PRJNA717768 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14083009.fastq.gz	Fastqsanger.gz
	SRR14083010.fastq.gz	Fastqsanger.gz
	SRR14083011.fastq.gz	Fastqsanger.gz
	SRR14083012.fastq.gz	Fastqsanger.gz
	SRR14083013.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Mitohormesis reprograms macrophage metabolism to enforce tolerance.

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance.

| PRJNA717764 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_OHestrogen_RNAseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_OHestrogen_RNAseq]

| PRJNA717769 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_tolerance_RNAseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_tolerance_RNAseq]

| PRJNA717771 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_ChIPseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_ChIPseq]

| PRJNA717767 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

Project description:Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

| PRJNA717768 | ENA

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_ChIPseq]

Project description:Macrophages generate mitochondrial reactive oxygen and electrophilic species (mtROS, mtRES) as antimicrobials during Toll-like receptor (TLR)-dependent inflammatory responses. Whether mitochondrial stress caused by these molecules impacts macrophage function is unknown. Here, we demonstrate that both pharmacologically- and lipopolysaccharide (LPS)-driven mitochondrial stress in macrophages triggers a stress response called mitohormesis. LPS-driven mitohormetic stress adaptations occur as macrophages transition from an LPS-responsive to LPS-tolerant state where stimulus-induced proinflammatory gene transcription is impaired, suggesting tolerance is a product of mitohormesis. Indeed, like LPS, hydroxyestrogen-triggered mitohormesis suppresses mitochondrial oxidative metabolism and acetyl-CoA production needed for histone acetylation and proinflammatory gene transcription, and is sufficient to enforce an LPS-tolerant state. Thus, mtROS and mtRES are TLR-dependent signaling molecules that trigger mitohormesis as a negative feedback mechanism to restrain inflammation via tolerance. Moreover, bypassing TLR signaling and pharmacologically triggering mitohormesis represents a novel anti-inflammatory strategy that co-opts this stress response to impair epigenetic support of proinflammatory gene transcription by mitochondria.

2021-04-04 | GSE169729 | GEO