Modulating Sema3A signal with a L1 mimetic peptide is not sufficient to promote motor recovery and axon regeneration after spinal cord injury
| العنوان: | Modulating Sema3A signal with a L1 mimetic peptide is not sufficient to promote motor recovery and axon regeneration after spinal cord injury |
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| المؤلفون: | Lyn B. Jakeman, Nicole Thomasset, Geneviève Rougon, Erik Mire |
| المساهمون: | Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS) |
| المصدر: | Molecular and Cellular Neuroscience Molecular and Cellular Neuroscience, Elsevier, 2008, 37 (2), pp.222-35 Molecular and Cellular Neuroscience, 2008, 37 (2), pp.222-35 |
| بيانات النشر: | Elsevier BV, 2008. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | Growth Cones, Neural Cell Adhesion Molecule L1, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, Article, Cell Line, Lesion, Mice, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, Semaphorin, Neural Pathways, medicine, Animals, Humans, Treatment Failure, Axon, Growth cone, Molecular Biology, Spinal cord injury, Cells, Cultured, Spinal Cord Injuries, 030304 developmental biology, Feedback, Physiological, 0303 health sciences, Regeneration (biology), Semaphorin-3A, SEMA3A, Recovery of Function, Cell Biology, medicine.disease, Spinal cord, Immunohistochemistry, Axons, Neuropilin-1, Peptide Fragments, Nerve Regeneration, Mice, Inbred C57BL, medicine.anatomical_structure, Spinal Cord, nervous system, Female, medicine.symptom, Neuroscience, 030217 neurology & neurosurgery |
| الوصف: | We examined whether Sema3A, which is upregulated at the site of spinal cord injury, exerts a direct effect on axons. We used ASNKL peptide that prevents specifically the inhibitory effect of Sema3A on L1/Neuropilin1 (Nrp1)-expressing axons. In the naïve mouse spinal cord, L1 is located on a subset of corticospinal axons, whereas Nrp1 is barely detectable. After contusion injury, Nrp1 is found on L1-negative immune cells, whereas its expression does not increase on severed axons. L1-expressing axons sprout extensively into the lesion site but no difference in axon density could be detected in the lesion area of mice treated with ASNKL. In agreement, these mice did not recover a better motor function than controls. Similarly, culture of neurons sensitive to ASNKL on cryosections of lesioned spinal cords revealed no effect of Sema3A. Our data indicate a limited direct effect of Sema3A on axonal growth at the site of a contusion injury, and suggest that alternative mechanisms underlie positive effects of Sema3A inhibition on motor recovery. |
| تدمد: | 1044-7431 1095-9327 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::23683d27c7c9a657828cb3e1a3a87703Test https://doi.org/10.1016/j.mcn.2007.09.009Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....23683d27c7c9a657828cb3e1a3a87703 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10447431 10959327 |
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