Evidence map›Paper›PMID 35998585›Full record

ArticleDevelopmental cell2022

DNGR-1-tracing marks an ependymal cell subset with damage-responsive neural stem cell potential.

Bruno Frederico, Isaura Martins, Diana Chapela, Francesca Gasparrini, Probir Chakravarty, Tobias Ackels, Cécile Piot, Bruna Almeida, Joana Carvalho, Alessandro Ciccarelli and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 8% of its field
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

13 citing papers in PubMed, 25 citations in OpenAlex.

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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

17 authors at 2 institutions in 2 countries.

Bruno FredericoImmunobiology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK. Electronic address: bruno.frederico@crick.ac.uk.
Isaura MartinsInstituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, 1649-028 Lisboa, Portugal.
Diana ChapelaInstituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, 1649-028 Lisboa, Portugal; TechnoPhage, SA, Av. Prof. Egas Moniz, 1649-028 Lisboa, Portugal.
Francesca GasparriniImmunobiology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Probir ChakravartyBioinformatics and Biostatistics, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Tobias AckelsSensory Circuits and Neurotechnology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Cécile PiotImmunobiology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Bruna AlmeidaExperimental Histopathology, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Joana CarvalhoExperimental Histopathology, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Alessandro CiccarelliAdvanced Light Microscopy, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Christopher J PeddieElectron Microscopy, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Neil RogersImmunobiology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
James BriscoeDevelopmental Dynamic Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
François GuillemotNeural Stem Cell Biology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Andreas T SchaeferSensory Circuits and Neurotechnology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK; Department of Neuroscience, Physiology &Pharmacology, University College London, London, UK.
Leonor SaúdeInstituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, 1649-028 Lisboa, Portugal; Instituto de Medicina Molecular e Instituto de Histologia e Biologia do Desenvolvimento, Faculdade de Medicina da Universidade de Lisboa, 1649-028 Lisboa, Portugal.
Caetano Reis e SousaImmunobiology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK. Electronic address: caetano@crick.ac.uk.
The Francis Crick Institute · GBUniversity of Lisbon · PT

Funding

Cancer Research UK FC001136Medical Research Council FC001136Wellcome Trust FC001136Wellcome Trust WT106973/Z/15/Z
6 · The paper itself

Abstract

Cells with latent stem ability can contribute to mammalian tissue regeneration after damage. Whether the central nervous system (CNS) harbors such cells remains controversial. Here, we report that DNGR-1 lineage tracing in mice identifies an ependymal cell subset, wherein resides latent regenerative potential. We demonstrate that DNGR-1-lineage-traced ependymal cells arise early in embryogenesis (E11.5) and subsequently spread across the lining of cerebrospinal fluid (CSF)-filled compartments to form a contiguous sheet from the brain to the end of the spinal cord. In the steady state, these DNGR-1-traced cells are quiescent, committed to their ependymal cell fate, and do not contribute to neuronal or glial lineages. However, trans-differentiation can be induced in adult mice by CNS injury or in vitro by culture with suitable factors. Our findings highlight previously unappreciated ependymal cell heterogeneity and identify across the entire CNS an ependymal cell subset wherein resides damage-responsive neural stem cell potential.

Indexed as

Neural Stem CellsAnimalsCell DifferentiationEpendymaMammalsMiceNeurogliaSpinal CordCLEC9Adendritic cellsependymal cellsneural stem cellstissue repair

Identifiers

PMID35998585
PMCPMC9616800
OpenAlexW4292633992

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.