Evidence map›Paper›PMID 29525572›Full record

ArticleEBioMedicine2018

Endogenous Mobilization of Bone-Marrow Cells Into the Murine Retina Induces Fusion-Mediated Reprogramming of Müller Glia Cells.

Martina Pesaresi, Sergi A Bonilla-Pons, Giacoma Simonte, Daniela Sanges, Umberto Di Vicino, Maria Pia Cosma

Abstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Review
  2. Cell Fusion in Reprogramming and Regeneration.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Neuronal-Hematopoietic Cell Fusion in Diabetic Neuropathy.Stem cells translational medicine · 2023
    Article
  8. Article
  9. Article
  10. Müller Glia-Mediated Retinal Regeneration.Molecular neurobiology · 2021
    Review
  11. Review
  12. Article
  13. Digesting the Importance of Cell Fusion in the Intestine.Cellular and molecular gastroenterology and hepatology · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Martina PesaresiCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.
Sergi A Bonilla-PonsCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.; Universitat de Barcelona (UB), Barcelona, Spain.
Giacoma SimonteCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.
Daniela SangesCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.
Umberto Di VicinoCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.
Maria Pia CosmaCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain.; ICREA, Barcelona, Spain.. Electronic address: pia.cosma@crg.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Cellular ReprogrammingAmacrine CellsAnimalsBone Marrow CellsCell DedifferentiationCell FusionCell ProliferationChemokine CXCL12Mice, TransgenicNeurogliaN-MethylaspartateReceptors, CXCR4RetinaRetinal Ganglion CellsSignal TransductionChemokine CXCL12Cxcl12 protein, mouseN-MethylaspartateReceptors, CXCR4Bone-marrow cellsCell fusion-mediated reprogrammingEndogenous migrationMüller glial cellsNMDA-damageRetinal damageSDF1/CXCR4 pathway

Identifiers

PMID29525572
PMCPMC5952225

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.