Evidence map›Paper›PMID 28904214›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

After Nerve Injury, Lineage Tracing Shows That Myelin and Remak Schwann Cells Elongate Extensively and Branch to Form Repair Schwann Cells, Which Shorten Radically on Remyelination.

Jose A Gomez-Sanchez, Kjara S Pilch, Milou van der Lans, Shaline V Fazal, Cristina Benito, Laura J Wagstaff, Rhona Mirsky, Kristjan R Jessen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% 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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 282 citations in OpenAlex.

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  15. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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117 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Jose A Gomez-SanchezDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.ORCID 0000-0002-6746-1800
Kjara S PilchDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.ORCID 0000-0003-2145-2535
Milou van der LansDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Shaline V FazalDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.ORCID 0000-0002-2813-4022
Cristina BenitoDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Laura J WagstaffDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Rhona MirskyDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom k.jessen@ucl.ac.uk r.mirsky@ucl.ac.uk.
Kristjan R JessenDepartment of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom k.jessen@ucl.ac.uk r.mirsky@ucl.ac.uk.
University College London · GB

Funding

Medical Research Council G0600967Wellcome Trust
6 · The paper itself

Abstract

There is consensus that, distal to peripheral nerve injury, myelin and Remak cells reorganize to form cellular columns, Bungner's bands, which are indispensable for regeneration. However, knowledge of the structure of these regeneration tracks has not advanced for decades and the structure of the cells that form them, denervated or repair Schwann cells, remains obscure. Furthermore, the origin of these cells from myelin and Remak cells and their ability to give rise to myelin cells after regeneration has not been demonstrated directly, although these conversions are believed to be central to nerve repair. Using genetic lineage-tracing and scanning-block face electron microscopy, we show that injury of sciatic nerves from mice of either sex triggers extensive and unexpected Schwann cell elongation and branching to form long, parallel processes. Repair cells are 2- to 3-fold longer than myelin and Remak cells and 7- to 10-fold longer than immature Schwann cells. Remarkably, when repair cells transit back to myelinating cells, they shorten ∼7-fold to generate the typically short internodes of regenerated nerves. The present experiments define novel morphological transitions in injured nerves and show that repair Schwann cells have a cell-type-specific structure that differentiates them from other cells in the Schwann cell lineage. They also provide the first direct evidence using genetic lineage tracing for two basic assumptions in Schwann cell biology: that myelin and Remak cells generate the elongated cells that build Bungner bands in injured nerves and that such cells can transform to myelin cells after regeneration.

Indexed as

Neuronal OutgrowthAnimalsFemaleMaleMiceMice, TransgenicMyelin SheathNerve RegenerationPeripheral Nerve InjuriesSchwann CellsinjurynervePNSregenerationremyelinationSchwann cell

Identifiers

PMID28904214
PMCPMC5597985
OpenAlexW2743621029

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.