ArticlePloS one2015
MASH1/Ascl1a leads to GAP43 expression and axon regeneration in the adult CNS.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- Scorpion (Hottentotta tamulus) venom pre-exposure delays functional recovery in mice following peripheral nerve injury.PloS one · 2025Article
- The transcription factor Jun is necessary for optic nerve regeneration in larval zebrafish.PloS one · 2025Article
- Deletion of Slc1a4 Suppresses Single Mauthner Cell Axon Regeneration In Vivo through Growth-Associated Protein 43.International journal of molecular sciences · 2024Article
- Single-cell analysis of innate spinal cord regeneration identifies intersecting modes of neuronal repair.Nature communications · 2024Article
- Histone methyltransferase Ezh2 coordinates mammalian axon regeneration via regulation of key regenerative pathways.The Journal of clinical investigation · 2024Article
- Serum response factor promotes axon regeneration following spinal cord transection injury.Neural regeneration research · 2023Article
- Circuit formation in the adult brain.The European journal of neuroscience · 2022Review
- Analysis of neuronal injury transcriptional response identifies CTCF and YY1 as co-operating factors regulating axon regeneration.Frontiers in molecular neuroscience · 2022Article
- Distal Axonal Proteins and Their Related MiRNAs in Cultured Cortical Neurons.Molecular neurobiology · 2019Article
- Regenerative capacity in the lamprey spinal cord is not altered after a repeated transection.PloS one · 2019Article
- Common genetic variants in GAL, GAP43 and NRSN1 and interaction networks confer susceptibility to Hirschsprung disease.Journal of cellular and molecular medicine · 2018Article
- Review
- Enhanced Neuronal Regeneration in the CAST/Ei Mouse Strain Is Linked to Expression of Differentiation Markers after Injury.Cell reports · 2017Article
- Selecting optimal combinations of transcription factors to promote axon regeneration: Why mechanisms matter.Neuroscience letters · 2017Review
- Protection of FK506 against neuronal apoptosis and axonal injury following experimental diffuse axonal injury.Molecular medicine reports · 2017Article
- The Effects of IGF-1 on TNF-α-Treated DRG Neurons by Modulating ATF3 and GAP-43 Expression via PI3K/Akt/S6K Signaling Pathway.Neurochemical research · 2017Article
- Gene Manipulation Strategies to Identify Molecular Regulators of Axon Regeneration in the Central Nervous System.Frontiers in cellular neuroscience · 2017Review
- AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury.Neural plasticity · 2017Article
- Reconnecting Eye to Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Review
- MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection.Scientific reports · 2016Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Unlike CNS neurons in adult mammals, neurons in fish and embryonic mammals can regenerate their axons after injury. These divergent regenerative responses are in part mediated by the growth-associated expression of select transcription factors. The basic helix-loop-helix (bHLH) transcription factor, MASH1/Ascl1a, is transiently expressed during the development of many neuronal subtypes and regulates the expression of genes that mediate cell fate determination and differentiation. In the adult zebrafish (Danio rerio), Ascl1a is also transiently expressed in retinal ganglion cells (RGCs) that regenerate axons after optic nerve crush. Utilizing transgenic zebrafish with a 3.6 kb GAP43 promoter that drives expression of an enhanced green fluorescent protein (EGFP), we observed that knock-down of Ascl1a expression reduces both regenerative gap43 gene expression and axonal growth after injury compared to controls. In mammals, the development of noradrenergic brainstem neurons requires MASH1 expression. In contrast to zebrafish RGCs, however, MASH1 is not expressed in the mammalian brainstem after spinal cord injury (SCI). Therefore, we utilized adeno-associated viral (AAV) vectors to overexpress MASH1 in four month old rat (Rattus norvegicus) brainstem neurons in an attempt to promote axon regeneration after SCI. We discovered that after complete transection of the thoracic spinal cord and implantation of a Schwann cell bridge, animals that express MASH1 exhibit increased noradrenergic axon regeneration and improvement in hindlimb joint movements compared to controls. Together these data demonstrate that MASH1/Ascl1a is a fundamental regulator of axonal growth across vertebrates and can induce modifications to the intrinsic state of neurons to promote functional regeneration in response to CNS injury.
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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.