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
  • dc.date.accessioned 2019-11-13T11:18:45Z
  • dc.date.available 2019-11-13T11:18:45Z
  • dc.date.issued 2018
  • 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.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.doi http://dx.doi.org/10.1016/j.ebiom.2018.02.023
  • dc.identifier.issn 2352-3964
  • dc.identifier.uri http://hdl.handle.net/10230/42837
  • 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.accessRights info:eu-repo/semantics/openAccess
  • dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0/
  • 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.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.type.version info:eu-repo/semantics/publishedVersion

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