Blood vessels guide Schwann cell migration in the adult demyelinated CNS through Eph/ephrin signaling.

Schwann cells (SC) enter the central nervous system (CNS) in pathophysiological conditions. However, how SC invade the CNS to remyelinate central axons remains undetermined. We studied SC migratory behavior ex vivo and in vivo after exogenous transplantation in the demyelinated spinal cord. The data...

ver descrição completa

Detalhes bibliográficos
Autores: Garcia-Diaz, Beatriz, Bachelin, Corinne, Coulpier, Fanny, Gerschenfeld, Gaspard, Deboux, Cyrille, Zujovic, Violetta, Charnay, Patrick, Topilko, Piotr, Baron-Van Evercooren, Anne
Formato: artículo
Fecha de publicación:2019
País:España
Recursos:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/17854
Acesso em linha:http://hdl.handle.net/20.500.12105/17854
Access Level:acceso abierto
Palavra-chave:Blood vessels
Central nervous system
EphrinB3
Migration
Schwann cells
Animals
Blood Vessels
Cell Movement
Demyelinating Diseases
Ephrin-B3
Female
Fibronectins
Mice
Mice, Inbred C57BL
Mice, Transgenic
Remyelination
Schwann Cells
Signal Transduction
Spinal Cord
Descrição
Resumo:Schwann cells (SC) enter the central nervous system (CNS) in pathophysiological conditions. However, how SC invade the CNS to remyelinate central axons remains undetermined. We studied SC migratory behavior ex vivo and in vivo after exogenous transplantation in the demyelinated spinal cord. The data highlight for the first time that SC migrate preferentially along blood vessels in perivascular extracellular matrix (ECM), avoiding CNS myelin. We demonstrate in vitro and in vivo that this migration route occurs by virtue of a dual mode of action of Eph/ephrin signaling. Indeed, EphrinB3, enriched in myelin, interacts with SC Eph receptors, to drive SC away from CNS myelin, and triggers their preferential adhesion to ECM components, such as fibronectin via integrinβ1 interactions. This complex interplay enhances SC migration along the blood vessel network and together with lesion-induced vascular remodeling facilitates their timely invasion of the lesion site. These novel findings elucidate the mechanism by which SC invade and contribute to spinal cord repair.

Registos relacionados