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NAPRT activation of macrophages

ABSTRACT: NAPRT activation of macrophages

PROVIDER: PRJNA559895 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9956040.fastq.gz	Fastqsanger.gz
	SRR9956041.fastq.gz	Fastqsanger.gz
	SRR9956042.fastq.gz	Fastqsanger.gz
	SRR9956043.fastq.gz	Fastqsanger.gz
	SRR9956044.fastq.gz	Fastqsanger.gz

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NAPRT activation of macrophages

Project description:Damage-associated molecular patterns (DAMPs) are molecules that can be actively or passively released by injured tissues and that activate the immune system. Here we show for the first time that the NAD biosynthetic enzyme nicotinate phosphoribosyltransferase (NAPRT), the rate-limiting enzymes in the intracellular synthesis of NAD from nicotinic acid, is physiologically present in human sera, where it acts as a novel DAMP. We detected NAPRT in plasma/sera from human donors by antibody-mediated luminex assays and mass spectrometry. Exposure of human and mouse macrophages to NAPRT triggers activation of ERK1/2, phosphorylation of IKKα/β and nuclear translocation of the p65 subunit of the NF-kB complex, with synthesis and secretion of inflammatory cytokines, including IL-1β, IL-8, TNFα and CCL3. Furthermore, NAPRT enhances monocyte differentiation into macrophages, by inducing macrophage colony-stimulating factor. These effects are independent of the NAPRT catalytic activity, but rely on the protein’s binding to TLR4, as demonstrated by showing direct in vitro interaction and by the in vivo lack of NAPRT effects in TLR4-/- macrophages. In line with the finding that NAPRT mediates endotoxin tolerance, sera from patients with sepsis or septic shock contain the highest levels of circulating NAPRT, compared to other chronic inflammatory conditions, including cancer. Importantly, patients with serum NAPRT >15 ng/ml are characterized by a worse clinical outcome, compared to the counterparts. Together, these data identify NAPRT as a novel endogenous ligand for TLR4 and a critical mediator of inflammation.

2019-08-13 | GSE135753 | GEO

Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [NAPRTKODSS]

Project description:NAPRT-mediated deamidated biosynthesis of nicotinamide adenine dinucleotide (NAD), an essential electron carrier for hundreds of biochemical reactions in all living cells, mediates the diet-microbe-host NAD metabolic interaction in mice. To study the function of this metabolic pathway in vivo, we recently generated a mutant mouse strain (NAPRT KO) in which a 21-nt fragment that encodes 7 amino acids in the catalytic domain of NAPRT was deleted in all cells using the CRISPR/Cas9-mediated gene editing technology. Our data showed that NAPRT KO mice are hypersensitive to DSS-induced colitis. To better understand this hypersensitivity at the molecular level, we analyzed transcriptomes of colon tissues from DSS-treated WT and NAPRT KO mice.

2025-12-06 | GSE271250 | GEO

Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [scWT2]

2025-12-06 | GSE271836 | GEO

Transcriptomic changes in the colon of WT and NAPRT KO mice after AOM injection [NAPRTKOAOM]

Project description:NAPRT-mediated deamidated biosynthesis of nicotinamide adenine dinucleotide (NAD), an essential electron carrier for hundreds of biochemical reactions in all living cells, mediates the diet-microbe-host NAD metabolic interaction in mice. To study the function of this metabolic pathway in vivo, we recently generated a mutant mouse strain (NAPRT KO) in which a 21-nt fragment that encodes 7 amino acids in the catalytic domain of NAPRT was deleted in all cells using the CRISPR/Cas9-mediated gene editing technology. Our results showed that NAPRT is highly expressed in the gut epithelial cells, where it functions to maintain the cellular NAD pool for an efficient response to stress-induced acute NAD depletion. Consistently, NAPRT deficiency impairs DNA repair, sensitizes mice to AOM-induced gut DNA damage. Here we profiled transcriptomic changes in the colon of WT and NAPRT KO mice at different time points after injection of AOM.

2025-12-06 | GSE271834 | GEO

Caspase-4 mediates SREBP1 activation in macrophages

Project description:Caspase-4 mediates SREBP1 activation in macrophages

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Kdm6a suppresses the alternative activation of macrophages

Project description:Kdm6a suppresses the alternative activation of macrophages

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NAPRT-mediated deamidated NAD biosynthesis enhances tissue resiliency and suppresses tumorigenesis

Project description:NAD biosynthetic enzymes are widely considered oncogenic due to their frequent overexpression in cancer to support elevated metabolic demand. This dataset is in support of a manuscript where we identify a tumor-suppressive role for the deamidated NAD biosynthesis pathway in both mice and humans. Unlike the ubiquitously expressed amidated salvage enzyme, NAPRT the first enzyme of the deamidated pathway is selectively enriched in gut epithelial cells, where it sustains NAD levels during stress-induced acute depletion. Loss of NAPRT compromises PARP activity and DNA repair, increasing susceptibility to chemically induced colitis, tumorigenesis, and age-associated spontaneous tumors in mice. Consistently, low NAPRT expression correlates with poor prognosis across multiple human cancers. These findings demonstrate that endogenous deamidated NAD biosynthesis suppresses tumorigenesis, and that enhancing this pathway may offer a strategy for tumor prevention.

2025-12-11 | MSV000100196 | MassIVE

Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

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Impact of LXR activation on alternatively activated human macrophages

Project description:Impact of LXR activation on alternatively activated human macrophages

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High salt primes a specific activation state of macrophages, M(Na)

Project description:Purpose: Investigate effects of high salt on human macrophage activation Methods: Human monocytes-derived macrophages were treated by additional 51mM NaCl for 24 hours (NaCl groups) or not (Control groups). mRNA profiles were generated by RNA-Seq, in triplicate, using Ion proton（Life tech). qRT–PCR validation was performed using SYBR Green assays. Results: High salt significantly promotes pro-inflammatory gene expressions,while suppresses the expressions of anti-inflammatory genes and pro-endocytic genes in human macrophages. Conclusions: Our results identify a novel macrophage activation state, M(Na), and high salt as a potential environmental risk factor for lung inflammation through the induction of M(Na) Human monocytes-derived macrophages were treated by additional 51mM NaCl for 24 hours (NaCl groups) or not (Control groups). mRNA profiles were generated by RNA-Seq, in triplicate, using Ion proton（Life tech). qRT–PCR validation was performed using SYBR Green assays.

2015-09-23 | E-GEOD-68482 | biostudies-arrayexpress

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