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The NAMPT/SIRT7/SOD2 axis regulates alveolar progenitor cell renewal and pulmonary fibrosis [scRNA-seq]

ABSTRACT: We employed single-cell RNA sequencing using the 10x Genomics platform to investigate the role of nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in NAD+ biosynthesis, in AT2 cells in the lung. NAMPT has been implicated in regulating stem cell function, mitochondrial bioenergetics, apoptosis, and senescence in neurodegenerative diseases, endothelial cells, and human iPS cells. Single-cell lung suspensions were prepared from Nampt AT2 conditional knockout and control mice at day 0 and day 4 post-bleomycin injury. scRNA-seq was performed on FACS-sorted Epcam+ and CD45+ live cells, and purified cells were clustered to evaluate NAMPT function in AT2 and immune cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE295739 | GEO | 2026/03/30

REPOSITORIES: GEO

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The NAMPT/SIRT7/SOD2 axis regulates alveolar progenitor cell renewal and pulmonary fibrosis [bulkRNA-seq]

Project description:We employed bulk RNA sequencing using the UCLA Technology Center for Genomics &Bioinformatics platform to investigate the role of nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in NAD+ biosynthesis, in AT2 cells in the lung. NAMPT has been implicated in regulating stem cell function, mitochondrial bioenergetics, apoptosis, and senescence in neurodegenerative diseases, endothelial cells, and human iPS cells. We used CRISPR/Cas9 system to knockout or activate NAMPT in immortalized IPF AT2 cells.

2026-03-30 | GSE295740 | GEO

The role of nicotinamide phosphoribosyltransferase (Nampt) in hippocampal neural stem/progenitor cells

Project description:Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age, but the molecular mechanisms responsible for these declines remain unclear. Here we show that levels of NAD+ and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD+ biosynthesis, decrease with age in the hippocampus. Ablation of Nampt in adult NSPCs reduced their pool and proliferation in vivo. The decrease in the NSPC pool during aging can be rescued by enhancing hippocampal NAD+ levels. Nampt is the main source of NSPC NAD+ levels and required for G1/S progression of the NSPC cell cycle. Nampt is also critical for oligodendrocytic lineage fate decisions through a mechanism mediated redundantly by Sirt1 and Sirt2. Ablation of Nampt in the adult NSPCs in vivo reduced NSPC-mediated oligodendrogenesis upon injury. These phenotypes recapitulate defects in NSPCs during aging, implicating Nampt-mediated NAD+ biosynthesis as a mediator of these age-associated functional declines. Total RNA obtained from neurospheres derived from postnatal hippocampi subjected to 48 hours in vitro of incubation with Nampt-specific inhibitor FK866 (10 nM, 4 samples) or vehicle (DMSO, 1:1000, 4 samples).

2014-05-08 | E-GEOD-49784 | biostudies-arrayexpress

NAMPT-dependent NAD+ biosynthesis controls circadian metabolism in a tissue-specific manner

Project description:Molecular clocks in the periphery coordinate tissue-specific daily biorhythms by integrating input from the hypothalamic master clock and intracellular metabolic signals. One such key metabolic signal is the cellular concentration of NAD+, which oscillates along with its biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT). NAD+ levels feed back into the clock to influence rhythmicity of biological functions, yet whether this metabolic fine-tuning occurs ubiquitously across cell types and is a core clock feature is unknown. Here we show that NAMPT-dependent control over the molecular clock varies substantially between tissues. Brown adipose tissue (BAT) requires NAMPT to sustain the amplitude of the core clock, whereas rhythmicity in white adipose tissue (WAT) is only moderately dependent on NAD+ biosynthesis and the skeletal muscle clock is completely refractory to loss of NAMPT. In BAT and WAT, NAMPT differentially orchestrates oscillation of clock-controlled gene networks and the diurnality of metabolite levels. NAMPT coordinates the rhythmicity of TCA cycle intermediates in BAT, but not WAT, and loss of NAD+ abolishes these oscillations similarly to high fat diet (HFD)-induced circadian disruption. Adipose NAMPT depletion also improved the ability of animals to defend body temperature during cold stress but this is independent of time-of-day. Thus, our findings reveal that peripheral molecular clocks and metabolic biorhythms are shaped in a highly tissue-specific manner by NAMPT-dependent NAD+ synthesis.

2023-04-11 | GSE221550 | GEO

G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients

Project description:Despite advancements in cancer therapies, bacterial complications remain a major challenge, delaying treatment and worsening outcomes. While immunosuppressive therapies and prolonged hospitalizations contribute, they do not fully explain the elevated infection risk in cancer patients. Here we show that tumors producing high levels of granulocyte colony-stimulating factor (G-CSF) promote the persistence of Gram-negative pathogens in head and neck squamous cell carcinoma. We identify tumor-driven activation of the nicotinamide phosphoribosyltransferase (NAMPT)- nicotinamide adenine dinucleotide (NAD) signaling axis in neutrophil progenitors, resulting in impaired phagocytosis and neutrophil extracellular traps formation, accelerated neutrophil aging, and buildup of tissue-damaging neutrophil subsets. This disrupts lung tissue integrity and facilitates bacterial persistence. Importantly, targeting the G-CSF-NAMPT pathway prevents the generation of dysfunctional neutrophils and improves bacterial clearance in vivo. Our findings reveal tumor-induced, NAMPT-dependent neutrophil reprogramming as a central driver of compromised antimicrobial defenses in cancer. Therapeutic strategies aimed at modulating G-CSF-NAMPT signaling could enhance infection control and survival for cancer patients

2025-10-17 | PXD069569 | Pride

G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients

2025-11-13 | PXD052631 | Pride

The role of nicotinamide phosphoribosyltransferase (Nampt) in hippocampal neural stem/progenitor cells

2014-05-08 | GSE49784 | GEO

The Interferon-inducible NAMPT acts as a protein phosphoribosylase to restrict viral infection

Project description:As obligate intracellular pathogens, viruses often activate host metabolic enzymes to supply intermediates that support progeny production. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the salvage NAD+ synthesis, is an interferon-inducible protein that inhibits the replication of several RNA and DNA viruses with unknown mechanism. Here we report that NAMPT restricts herpes simplex virus 1 (HSV-1) replication via phosphoribosyl-hydrolase activity toward key viral structural proteins, independent of NAD+ synthesis. Deep mining of enriched phosphopeptides of HSV-1-infected cells identified phosphoribosylated viral structural proteins, particularly glycoproteins and tegument proteins. Indeed, NAMPT dephosphoribosylates viral proteins in vitro and in cells. Chimeric and recombinant HSV-1 carrying phosphoribosylation-resistant mutations show that phosphoribosylation promotes the incorporation of structural proteins into HSV-1 virions and subsequent virus entry. Moreover, loss of NAMPT renders mice highly susceptible to HSV-1 infection. The work describes a hidden enzyme activity of a metabolic enzyme in viral infection and host defense, offering a system to interrogate roles of phosphoribosylation in metazoans.

2024-09-13 | PXD050684 | Pride

Olaparib induced NAMPT and circPTTG1IP expression promoted cell survival and contributed to drug resistance in glioblastoma cells

Project description:Glioblastoma (GBM) is an aggressive brain cancer that is notoriously resistant to chemotherapy, particularly to Temozolomide (TMZ). In this study, we examined a patient-derived TMZ-resistant GBM cell line and assessed the effects of the PARP inhibitor Olaparib. We observed that while Olaparib exhibited significant tumor inhibition, its required dosage exceeded clinically acceptable levels. Transcriptomic analysis revealed a notable upregulation of nicotinamide phosphoribosyltransferase (NAMPT) in the surviving tumor cells, suggesting that increased intracellular NAD+ levels contributed to their resistance against both Olaparib and TMZ. By optimizing the dosages of Olaparib and FK866, a NAMPT inhibitor, we were able to develop a combination therapy that effectively killed TMZ-resistant GBM cells while adhering to clinically applicable pharmacodynamic and toxicological standards for each drug. This combination was also tested across other TMZ-resistant cell lines and 3D organoids, showing promising potential for clinical application. Additionally, through profiling plasma-detectable circRNA species from the combination treatment, we identified circPTTG1IP as a potential biomarker with negative predictive value. Further analysis indicated that circPTTG1IP might regulate NAMPT expression and NAD+ levels, potentially through its interaction with miRNAs targeting NAMPT. This research provides insights into a novel therapeutic strategy for overcoming TMZ resistance in GBM.

2025-06-02 | GSE295766 | GEO

RNAi profiling of human MCF-7 cells depleted for NAMPT knockdown

Project description:NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.

2009-06-08 | E-GEOD-13449 | biostudies-arrayexpress

Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice

Project description:We evaluated the effects of NAMPT (nicotinamide phosphoribosyltransferase) knockout on transcriptome in brown adipose tissue (BAT) by analyzing BAT obtained from control (Nampt-flox/flox, F1-F4) and adipocyte-specific Nampt knockout (ANKO, A1-A4) mice.

2019-11-14 | GSE137149 | GEO

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