期刊
ACTA NEUROPATHOLOGICA
卷 138, 期 3, 页码 457-476出版社
SPRINGER
DOI: 10.1007/s00401-019-02011-1
关键词
Schwann cells; Central nervous system; Blood vessels; Migration; EphrinB3
资金
- Region Ile-de-France (NERF) [2011-45]
- Fondation pour la Recherche Medicale [DGE 20,111,123,023]
- Federation pour la Recherche sur le Cerveau - Rotary International France
- ICM Foundation
- National Multiple Sclerosis Society (NMSS) [RG 5088-A-1]
- INSERM, CNRS, ARSEP
- program Investissements d'Avenir [ANR-10-IAIHU-06]
- INSERM, CNRS, IBENS, the program Investissements d'Avenir [ANR-11-INBS-0011-NeurATRIS]
- France Genomique national infrastructure as part of the Investissements d'Avenir program [ANR-10-INBS-09]
- Junta de Andalucia
- European Commission under the Seventh Framework Programme of the European Union [291730, TAHUB-II-107]
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 integrin beta 1 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.
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