ArticleThe EMBO journal2016
NB-3 signaling mediates the cross-talk between post-traumatic spinal axons and scar-forming cells.
Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Biological engineering approaches for modulating the pathological microenvironment and promoting axonal regeneration after spinal cord injury.Frontiers in neuroscience · 2025Review
- Dual electrical stimulation at spinal-muscular interface reconstructs spinal sensorimotor circuits after spinal cord injury.Nature communications · 2024Article
- Restoring Cellular Energetics Promotes Axonal Regeneration and Functional Recovery after Spinal Cord Injury.Cell metabolism · 2020Article
- Cell Adhesion Molecules and Protein Synthesis Regulation in Neurons.Frontiers in molecular neuroscience · 2020Review
- Highly Sensitive Microstructure-Based Flexible Pressure Sensor for Quantitative Evaluation of Motor Function Recovery after Spinal Cord Injury.Sensors (Basel, Switzerland) · 2019Article
- Roles of mTOR Signaling in Tissue Regeneration.Cells · 2019Review
- Latrophilin's Social Protein Network.Frontiers in neuroscience · 2019Review
- Cell Adhesion Molecule Close Homolog of L1 (CHL1) Guides the Regrowth of Regenerating Motor Axons and Regulates Synaptic Coverage of Motor Neurons.Frontiers in molecular neuroscience · 2018Article
- NB-3 signaling mediates the cross-talk between post-traumatic spinal axons and scar-forming cells.The EMBO journal · 2016Article
- Messages from forgotten friends: classic cell adhesion molecules inhibit regeneration too.The EMBO journal · 2016Article
- Association of Cell Adhesion Molecules Contactin-6 and Latrophilin-1 Regulates Neuronal Apoptosis.Frontiers in molecular neuroscience · 2016Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known about the molecules mediating the cross-talk between post-traumatic axons and scar-forming cells after spinal cord injury. We found that a sustained NB-3 induction was simultaneously present in the terminations of post-traumatic corticospinal axons and scar-forming cells at the spinal lesion site, where they were in direct contact when axons tried to penetrate the glial scar. The regrowth of corticospinal axons was enhanced in vivo with NB-3 deficiency or interruption of NB-3 trans-homophilic interactions. Biochemical, in vitro and in vivo evidence demonstrated that NB-3 homophilically interacted in trans to initiate a growth inhibitory signal transduction from scar-forming cells to neurons by modulating mTOR activity via CHL1 and PTPσ. NB-3 deficiency promoted BMS scores, electrophysiological transmission, and synapse reformation between regenerative axons and neurons. Our findings demonstrate that NB-3 trans-homophilic interactions mediate the cross-talk between post-traumatic axons and scar-forming cells and impair the intrinsic growth ability of injured axons.
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