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Mitohormesis reprograms macrophage metabolism to enforce tolerance.

ABSTRACT: Mitohormesis reprograms macrophage metabolism to enforce tolerance.

PROVIDER: PRJNA717764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14083003.fastq.gz	Fastqsanger.gz
	SRR14083004.fastq.gz	Fastqsanger.gz
	SRR14083005.fastq.gz	Fastqsanger.gz
	SRR14083006.fastq.gz	Fastqsanger.gz
	SRR14083007.fastq.gz	Fastqsanger.gz

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Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_ChIPseq]

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

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Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_OHestrogen_RNAseq]

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Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

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Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_tolerance_RNAseq]

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

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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

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_OHestrogen_RNAseq]

2021-04-04 | GSE169727 | GEO

Mitohormesis reprograms macrophage metabolism to enforce tolerance [vWAT_mac_RNAseq]

2021-04-04 | GSE169728 | GEO

Mitohormesis reprograms macrophage metabolism to enforce tolerance [BMDM_tolerance_RNAseq]

2021-04-04 | GSE169730 | GEO

Mitohormesis reprograms macrophage metabolism to enforce tolerance.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-04-04 | GSE169731 | GEO

Mitohormesis reprogrammes macrophage metabolism to enforce tolerance.

Project description:Macrophages generate mitochondrial reactive oxygen species and mitochondrial reactive electrophilic species 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 driven 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 wherein stimulus-induced pro-inflammatory gene transcription is impaired, suggesting tolerance is a product of mitohormesis. Indeed, like LPS, hydroxyoestrogen-triggered mitohormesis suppresses mitochondrial oxidative metabolism and acetyl-CoA production needed for histone acetylation and pro-inflammatory gene transcription, and is sufficient to enforce an LPS-tolerant state. Thus, mitochondrial reactive oxygen species and mitochondrial reactive electrophilic species are TLR-dependent signalling molecules that trigger mitohormesis as a negative feedback mechanism to restrain inflammation via tolerance. Moreover, bypassing TLR signalling and pharmacologically triggering mitohormesis represents a new anti-inflammatory strategy that co-opts this stress response to impair epigenetic support of pro-inflammatory gene transcription by mitochondria.

| S-EPMC8162914 | biostudies-literature

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