title: NB-3 signaling mediates the cross-talk between post-traumatic spinal axons and scar-forming cells.
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.
authors.affiliation: Institute of Neuroscience, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, China.
authors.forename: Zhenhui
authors.initials: Z
authors.lastname: Huang
authors.affiliation: Institute of Neuroscience, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, China.
authors.forename: Yarong
authors.initials: Y
authors.lastname: Gao
authors.affiliation: Institute of Neuroscience, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, China.
authors.forename: Yuhui
authors.initials: Y
authors.lastname: Sun
authors.affiliation: The Medical School of Lanzhou University, Lanzhou, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Institute of Neuroscience, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Yin
authors.affiliation: Department of Bioengineering, Nagaoka University of Technology, Niigata, Japan.
authors.forename: Yasushi
authors.identifier: 0000-0001-9230-6784
authors.initials: Y
authors.lastname: Shimoda
authors.affiliation: National Institute of Technology, Nagaoka College, Niigata, Japan.
authors.forename: Kazutada
authors.initials: K
authors.lastname: Watanabe
authors.affiliation: Institute of Neuroscience, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, China liuyaobo@suda.edu.cn.
authors.forename: Yaobo
authors.identifier: 0000-0002-7663-5649
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology*; D015816:Cell Adhesion Molecules, Neuronal / Q000378:metabolism*; D002450:Cell Communication; D002921:Cicatrix / Q000473:pathology*; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D009457:Neuroglia / Q000502:physiology*; D015398:Signal Transduction; D013119:Spinal Cord Injuries / Q000473:pathology*
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; C526283:contactin 6 protein, mouse
keywords: NB‐3; axonal regeneration; spinal cord injury