Identification of a discrete subpopulation of spinal cord ependymal cells with neural stem cell properties
Stenudd, Moa; Sabelström, Hanna; Llorens-Bobadilla, Enric; Zamboni, Margherita; Blom, Hans; Brismar, Hjalmar; Zhang, Shupei; Basak, Onur; Clevers, Hans; Göritz, Christian; Barnabé-Heider, Fanie; Frisén, Jonas
(2022) Cell Reports, volume 38, issue 9, pp. 1 - 16
(Article)
Abstract
Spinal cord ependymal cells display neural stem cell properties in vitro and generate scar-forming astrocytes and remyelinating oligodendrocytes after injury. We report that ependymal cells are functionally heterogeneous and identify a small subpopulation (8% of ependymal cells and 0.1% of all cells in a spinal cord segment), which we denote
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ependymal A (EpA) cells, that accounts for the in vitro stem cell potential in the adult spinal cord. After spinal cord injury, EpA cells undergo self-renewing cell division as they give rise to differentiated progeny. Single-cell transcriptome analysis revealed a loss of ependymal cell gene expression programs as EpA cells gained signaling entropy and dedifferentiated to a stem-cell-like transcriptional state after an injury. We conclude that EpA cells are highly differentiated cells that can revert to a stem cell state and constitute a therapeutic target for spinal cord repair.
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Keywords: EpA cells, ependymal cells, neural stem cells, spinal cord injury, Neural Stem Cells/metabolism, Cell Differentiation/physiology, Humans, Neuroglia, Spinal Cord/metabolism, Spinal Cord Injuries/metabolism, General Biochemistry,Genetics and Molecular Biology, Research Support, Non-U.S. Gov't, Journal Article
ISSN: 2211-1247
Publisher: Cell Press
Note: Funding Information: We thank M. Djelloul and X. Li for discussions, J.E. Goldman for the O4 antibody, and M. Wegner for the Myrf antibody. This study was supported by grants from the Swedish Research Council , the Swedish Cancer Society , the Swedish Foundation for Strategic Research , Knut och Alice Wallenbergs Stiftelse , and the IRP Schellenberg Foundation. E.L.-B. was supported by an IRP Schellenberg Foundation postdoctoral fellowship. Publisher Copyright: © 2022 The Author(s)
(Peer reviewed)