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Sci Rep. 2017 Jan 24;7:41122. doi: 10.1038/srep41122.

Ependymal cell contribution to scar formation after spinal cord injury is minimal, local and dependent on direct ependymal injury.

Author information

1
Divison of Spine Surgery, Department of Orthopaedics, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.
2
Department of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
3
Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
4
Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27607, USA.

Abstract

Ependyma have been proposed as adult neural stem cells that provide the majority of newly proliferated scar-forming astrocytes that protect tissue and function after spinal cord injury (SCI). This proposal was based on small, midline stab SCI. Here, we tested the generality of this proposal by using a genetic knock-in cell fate mapping strategy in different murine SCI models. After large crush injuries across the entire spinal cord, ependyma-derived progeny remained local, did not migrate and contributed few cells of any kind and less than 2%, if any, of the total newly proliferated and molecularly confirmed scar-forming astrocytes. Stab injuries that were near to but did not directly damage ependyma, contained no ependyma-derived cells. Our findings show that ependymal contribution of progeny after SCI is minimal, local and dependent on direct ependymal injury, indicating that ependyma are not a major source of endogenous neural stem cells or neuroprotective astrocytes after SCI.

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