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Endogenous mobilization of bone-marrow cells into the murine retina induces fusion-mediated reprogramming of müller glia cells

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dc.contributor.author Pesaresi, Martina
dc.contributor.author Bonilla-Pons, Sergi A.
dc.contributor.author Simonte, Giacoma, 1984-
dc.contributor.author Sanges, Daniela
dc.contributor.author Di Vicino, Umberto
dc.contributor.author Cosma, Maria Pia, 1970-
dc.date.accessioned 2019-11-13T11:18:45Z
dc.date.available 2019-11-13T11:18:45Z
dc.date.issued 2018
dc.identifier.citation Pesaresi M, Bonilla-Pons SA, Simonte G, Sanges D, Di Vicino U, Cosma MP. Endogenous mobilization of bone-marrow cells into the murine retina induces fusion-mediated reprogramming of müller glia cells. EBioMedicine. 2018; 30:38-51. DOI 10.1016/j.ebiom.2018.02.023
dc.identifier.issn 2352-3964
dc.identifier.uri http://hdl.handle.net/10230/42837
dc.description.abstract Müller glial cells (MGCs) represent the most plastic cell type found in the retina. Following injury, zebrafish and avian MGCs can efficiently re-enter the cell cycle, proliferate and generate new functional neurons. The regenerative potential of mammalian MGCs, however, is very limited. Here, we showed that N-methyl-d-aspartate (NMDA) damage stimulates murine MGCs to re-enter the cell cycle and de-differentiate back to a progenitor-like stage. These events are dependent on the recruitment of endogenous bone marrow cells (BMCs), which, in turn, is regulated by the stromal cell-derived factor 1 (SDF1)-C-X-C motif chemokine receptor type 4 (CXCR4) pathway. BMCs mobilized into the damaged retina can fuse with resident MGCs, and the resulting hybrids undergo reprogramming followed by re-differentiation into cells expressing markers of ganglion and amacrine neurons. Our findings constitute an important proof-of-principle that mammalian MGCs retain their regenerative potential, and that such potential can be activated via cell fusion with recruited BMCs. In this perspective, our study could contribute to the development of therapeutic strategies based on the enhancement of mammalian endogenous repair capabilities.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Elsevier
dc.relation.ispartof EBioMedicine. 2018; 30:38-51
dc.rights © 2018 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license(http://creativecommons.org/licenses/by-nc-nd/4.0/)
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.title Endogenous mobilization of bone-marrow cells into the murine retina induces fusion-mediated reprogramming of müller glia cells
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1016/j.ebiom.2018.02.023
dc.subject.keyword Retinal damage
dc.subject.keyword NMDA-damage
dc.subject.keyword Müller glial cells
dc.subject.keyword Cell fusion-mediated reprogramming
dc.subject.keyword Bone-marrow cells
dc.subject.keyword Endogenous migration
dc.subject.keyword SDF1/CXCR4 pathway
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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