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Journal article
EphB3 receptors function as dependence receptors to mediate oligodendrocyte cell death following contusive spinal cord injury
Cell death & disease, v 6(10), pp e1922-e1922
15 Oct 2015
PMID: 26469970
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
We demonstrate that EphB3 receptors mediate oligodendrocyte (OL) cell death in the injured spinal cord through dependence receptor mechanism. OLs in the adult spinal cord express EphB3 as well as other members of the Eph receptor family. Spinal cord injury (SCI) is associated with tissue damage, cellular loss and disturbances in EphB3-ephrinB3 protein balance acutely (days) after the initial impact creating an environment for a dependence receptor-mediated cell death to occur. Genetic ablation of EphB3 promotes OL survival associated with increased expression of myelin basic protein and improved locomotor function in mice after SCI. Moreover, administration of its ephrinB3 ligand to the spinal cord after injury also promotes OL survival. Our in vivo findings are supported by in vitro studies showing that ephrinB3 administration promotes the survival of both oligodendroglial progenitor cells and mature OLs cultured under pro-apoptotic conditions. In conclusion, the present study demonstrates a novel dependence receptor role of EphB3 in OL cell death after SCI, and supports further development of ephrinB3-based therapies to promote recovery.
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Details
- Title
- EphB3 receptors function as dependence receptors to mediate oligodendrocyte cell death following contusive spinal cord injury
- Creators
- Y Tsenkina - Miami Project to Cure ParalysisJ Ricard - Drexel UniversityE Runko - Miami Project to Cure ParalysisM M Quiala-Acosta - The Miami Project to Cure Paralysis, The Department of Neurosurgery, Miller School of Medicine, The University of Miami, Miami, FL, USAJ Mier - Miami Project to Cure ParalysisD J Liebl - Miami Project to Cure Paralysis
- Publication Details
- Cell death & disease, v 6(10), pp e1922-e1922
- Publisher
- Springer Nature
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biology
- Web of Science ID
- WOS:000367150100026
- Scopus ID
- 2-s2.0-84975246076
- Other Identifier
- 991019168885104721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Cell Biology