ArticleScientific reports2016
Pre-B-cell colony-enhancing factor protects against apoptotic neuronal death and mitochondrial damage in ischemia.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- A sensory and motor neuropathy caused by a genetic variant ofScience advances · 2025Article
- Nicotinamide phosphoribosyltransferase in NADCell death discovery · 2025Review
- Article
- Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke.Neurochemical research · 2025Article
- Dietary NMN supplementation enhances motor and NMJ function in ALS.Experimental neurology · 2024Article
- Mechanisms of the NADFrontiers in cell and developmental biology · 2024Review
- Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs).Journal of visualized experiments : JoVE · 2022Article
- Metabolomic and transcriptional profiling reveals bioenergetic stress and activation of cell death and inflammatory pathwaysJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Astroglia Abnormalities in Post-stroke Mood Disorders.Advances in neurobiology · 2021Review
- Evaluation of the NADExperimental neurology · 2020Article
- The effect of NAMPT deletion in projection neurons on the function and structure of neuromuscular junction (NMJ) in mice.Scientific reports · 2020Article
- Subcellular NAMPT-mediated NADJournal of neurochemistry · 2019Article
- Targeting NAMPT as a therapeutic strategy against stroke.Stroke and vascular neurology · 2019Review
- Nicotinamide phosphoribosyltransferase contributes to cocaine addiction through sirtuin 1.International journal of physiology, pathophysiology and pharmacology · 2019Article
- Possible Involvement of PTEN Signaling Pathway in the Anti-apoptotic Effect of Electroacupuncture Following Ischemic Stroke in Rats.Cellular and molecular neurobiology · 2018Article
- Nicotinamide Adenine Dinucleotide Metabolism and Neurodegeneration.Antioxidants & redox signaling · 2018Review
- MicroRNA-125a-3p is involved in early behavioral disorders in stroke-afflicted rats through the regulation of Cadm2.International journal of molecular medicine · 2017Article
- Deletion of Nampt in Projection Neurons of Adult Mice Leads to Motor Dysfunction, Neurodegeneration, and Death.Cell reports · 2017Article
- Assessed and Emerging Biomarkers in Stroke and Training-Mediated Stroke Recovery: State of the Art.Neural plasticity · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We previously demonstrated that Pre-B-cell colony-enhancing factor (PBEF), also known as nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis pathway, plays a brain and neuronal protective role in ischemic stroke. In this study, we further investigated the mechanism of its neuroprotective effect after ischemia in the primary cultured mouse cortical neurons. Using apoptotic cell death assay, fluorescent imaging, molecular biology, mitochondrial biogenesis measurements and Western blotting analysis, our results show that the overexpression of PBEF in neurons can significantly promote neuronal survival, reduce the translocation of apoptosis inducing factor (AIF) from mitochondria to nuclei and inhibit the activation of capase-3 after glutamate-induced excitotoxicity. We further found that the overexpression of PBEF can suppress glutamate-induced mitochondrial fragmentation, the loss of mitochondrial DNA (mtDNA) content and the reduction of PGC-1 and NRF-1 expressions. Furthermore, these beneficial effects by PBEF are dependent on its enzymatic activity of NAD(+) synthesis. In summary, our study demonstrated that PBEF ameliorates ischemia-induced neuronal death through inhibiting caspase-dependent and independent apoptotic signaling pathways and suppressing mitochondrial damage and dysfunction. Our study provides novel insights into the mechanisms underlying the neuroprotective effect of PBEF, and helps to identify potential targets for ischemic stroke therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.