ArticleJournal of neuropathology and experimental neurology2014
Semaphorin 3A signaling through neuropilin-1 is an early trigger for distal axonopathy in the SOD1G93A mouse model of amyotrophic lateral sclerosis.
Article in Journal of neuropathology and experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Antibody-Based Therapeutic Interventions for Amyotrophic Lateral Sclerosis: A Systematic Literature Review.Frontiers in neuroscience · 2021Pooled it
- Neuronal guidance signaling in neurodegenerative diseases: Key regulators that function at neuron-glia and neuroimmune interfaces.Neural regeneration research · 2026Article
- Inflammatory cytokines disrupt astrocyte exosomal HepaCAM-mediated protection against neuronal excitotoxicity in the SOD1G93A ALS model.Science advances · 2024Article
- Pathomechanistic Networks of Motor System Injury in Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2024Review
- Skeletal muscle in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2023Review
- Early Alterations in Structural and Functional Properties in the Neuromuscular Junctions of Mutant FUS Mice.International journal of molecular sciences · 2023Article
- An increase in Semaphorin 3A biases the axonal direction and induces an aberrant dendritic arborization in an in vitro model of human neural progenitor differentiation.Cell & bioscience · 2022Article
- The Cellular and Molecular Signature of ALS in Muscle.Journal of personalized medicine · 2022Review
- Phosphorylated CRMP1, axon guidance protein, is a component of spheroids and is involved in axonal pathology in amyotrophic lateral sclerosis.Frontiers in neurology · 2022Article
- Comparing therapeutic modulators of the SOD1 G93A Amyotrophic Lateral Sclerosis mouse pathophysiology.Frontiers in neuroscience · 2022Article
- Modelling and Refining Neuronal Circuits with Guidance Cues: Involvement of Semaphorins.International journal of molecular sciences · 2021Review
- Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021Review
- Recent Advances on the Role of GSK3β in the Pathogenesis of Amyotrophic Lateral Sclerosis.Brain sciences · 2020Review
- Fyn Tyrosine Kinase as Harmonizing Factor in Neuronal Functions and Dysfunctions.International journal of molecular sciences · 2020Review
- The multifaceted role of kinases in amyotrophic lateral sclerosis: genetic, pathological and therapeutic implications.Brain : a journal of neurology · 2020Review
- CRMP2 mediates Sema3F-dependent axon pruning and dendritic spine remodeling.EMBO reports · 2020Article
- Mechanical stimulation of Schwann cells promote peripheral nerve regeneration via extracellular vesicle-mediated transfer of microRNA 23b-3p.Theranostics · 2020Article
- Neuropathy target esterase (NTE/PNPLA6) and organophosphorus compound-induced delayed neurotoxicity (OPIDN).Advances in neurotoxicology · 2020Article
- Omics Approach to Axonal Dysfunction of Motor Neurons in Amyotrophic Lateral Sclerosis (ALS).Frontiers in neuroscience · 2020Review
- Muscle secretion of toxic factors, regulated by miR126-5p, facilitates motor neuron degeneration in amyotrophic lateral sclerosis.Neural regeneration research · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a motor neuron disease characterized by progressive distal axonopathy that precedes actual motor neuron death. Triggers for neuromuscular junction degeneration remain to be determined, but the axon repulsion factor semaphorin 3A (Sema3A), which is derived from terminal Schwann cells, is a plausible candidate. This study examines the hypothesis that Sema3A signaling through its motor neuron neuropilin-1 (NRP1) receptor triggers distal axonopathy and muscle denervation in the SOD1 mouse model of ALS. Neuropilin-1 was found to be expressed in axonal terminals at the mouse neuromuscular junction in vivo and in NSC-34 motor neuron-like cells in vitro. In differentiated NSC-34 cells, an anti-NRP1 antibody that selectively blocks Sema3A binding to NRP1 prevented Sema3A-induced growth cone collapse. Furthermore, intraperitoneal injections of anti-NRP1 antibody administered twice weekly from age 40 days significantly delayed and even temporarily reversed motor functional decline while prolonging the life span of SOD1 mice. Histologic evaluation at 90 and 125 days revealed that anti-NRP1 antibody reduced neuromuscular junction denervation and attenuated pathologic alterations in ventral roots at late-stage disease. These data suggest that peripheral NRP1 signaling is involved in the pathobiology of this ALS model and that antagonizing Sema3A/NRP1 binding or downstream signals could have implications for the treatment of ALS.
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