ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Nicotinamide mononucleotide adenylyltransferase expression in mitochondrial matrix delays Wallerian degeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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101 citing papers in PubMed, 152 citations in OpenAlex.
- The Pof1 nicotinamide mononucleotide adenylyl transferase has a non-canonical role in NADThe Journal of biological chemistry · 2026Article
- Near infrared fluorophore specific for annexin A2 identifies peripheral nerve injury in a rodent transection model.Frontiers in cell and developmental biology · 2026Article
- FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NADRedox report : communications in free radical research · 2025Article
- REV-ERBα regulates brain NADNature aging · 2025Article
- The Roles of Moonlighting Nicotinamide Mononucleotide Adenylyl Transferases in Cell Physiology.International journal of molecular sciences · 2025Review
- Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.Biomolecules · 2024Review
- Identification and characterization ofClinical case reports · 2024Article
- Fertility protection during chemotherapy treatment by boosting the NAD(P)EMBO molecular medicine · 2024Article
- SARM1-Dependent Axon Degeneration: Nucleotide Signaling, Neurodegenerative Disorders, Toxicity, and Therapeutic Opportunities.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Role of NADCellular and molecular neurobiology · 2023Review
- Glycolytic System in Axons Supplement Decreased ATP Levels after Axotomy of the Peripheral Nerve.eNeuro · 2023Article
- Alpha-synucleinopathy reduces NMNAT3 protein levels and neurite formation that can be rescued by targeting the NAD+ pathway.Human molecular genetics · 2022Article
- Of axons that struggle to make ends meet: Linking axonal bioenergetic failure to programmed axon degeneration.Biochimica et biophysica acta. Bioenergetics · 2022Review
- NADInternational journal of molecular sciences · 2022Article
- Small Molecule Regulators Targeting NADCurrent medicinal chemistry · 2022Article
- Axonal spheroids in neurodegeneration.Molecular and cellular neurosciences · 2021Review
- Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- NADNature reviews. Molecular cell biology · 2021Review
- Advances of Glycometabolism Engineering in Chinese Hamster Ovary Cells.Frontiers in bioengineering and biotechnology · 2021Review
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
41 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies of naturally occurring mutant mice, wld(s), showing delayed Wallerian degeneration phenotype, suggest that axonal degeneration is an active process. We previously showed that increased nicotinamide adenine dinucleotide (NAD)-synthesizing activity by overexpression of nicotinamide mononucleotide adenylyltransferase (NMNAT) is the essential component of the Wld(s) protein, the expression of which is responsible for the delayed Wallerian degeneration phenotype in wld(s) mice. Indeed, NMNAT overexpression in cultured neurons provides robust protection to neurites, as well. To examine the effect of NMNAT overexpression in vivo and to analyze the mechanism that causes axonal protection, we generated transgenic mice (Tg) overexpressing NMNAT1 (nuclear isoform), NMNAT3 (mitochondrial isoform), or the Wld(s) protein bearing a W258A mutation, which disrupts NAD-synthesizing activity of the Wld(s) protein. Wallerian degeneration delay in NMNAT3-Tg was similar to that in wld(s) mice, whereas axonal protection in NMNAT1-Tg or Wld(s)(W258A)-Tg was not detectable. Detailed analysis of subcellular localization of the overexpressed proteins revealed that the axonal protection phenotype was correlated with localization of NMNAT enzymatic activity to mitochondrial matrix. Furthermore, we found that isolated mitochondria from mice showing axonal protection expressed unchanged levels of respiratory chain components, but were capable of increased ATP production. These results suggest that axonal protection by NMNAT expression in neurons is provided by modifying mitochondrial function. Alteration of mitochondrial function may constitute a novel tool for axonal protection, as well as a possible treatment of diseases involving axonopathy.
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