Evidence map›Paper›PMID 26494786›Full record

ArticleGenes & development2015

A cellular, molecular, and pharmacological basis for appendage regeneration in mice.

Thomas H Leung, Emily R Snyder, Yinghua Liu, Jing Wang, Seung K Kim

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. 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, 31 citations in OpenAlex.

  1. Article
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  11. p21Cartilage · 2021
    Article
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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

5 authors at 2 institutions in 1 country.

Thomas H LeungDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Dermatology, Stanford University School of Medicine, Stanford, California 94305, USA;
Emily R SnyderDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA;
Yinghua LiuDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA;
Jing WangDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA;
Seung K KimDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Medicine, Oncology Division, Stanford University School of Medicine, Stanford, California 94305, USA.
Stanford University · USStanford Medicine · US

Funding

Understanding Appendage Regeneration in MiceK08AR066661 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI LEUNG, THOMAS H. · 2014 to 2018
$839k
Howard Hughes Medical InstituteNIAMS NIH HHS AR066661NIAMS NIH HHS K08 AR066661
6 · The paper itself

Abstract

Regenerative medicine aims to restore normal tissue architecture and function. However, the basis of tissue regeneration in mammalian solid organs remains undefined. Remarkably, mice lacking p21 fully regenerate injured ears without discernable scarring. Here we show that, in wild-type mice following tissue injury, stromal-derived factor-1 (Sdf1) is up-regulated in the wound epidermis and recruits Cxcr4-expressing leukocytes to the injury site. In p21-deficient mice, Sdf1 up-regulation and the subsequent recruitment of Cxcr4-expressing leukocytes are significantly diminished, thereby permitting scarless appendage regeneration. Lineage tracing demonstrates that this regeneration derives from fate-restricted progenitor cells. Pharmacological or genetic disruption of Sdf1-Cxcr4 signaling enhances tissue repair, including full reconstitution of tissue architecture and all cell types. Our findings identify signaling and cellular mechanisms underlying appendage regeneration in mice and suggest new therapeutic approaches for regenerative medicine.

Indexed as

Cyclin-Dependent Kinase Inhibitor p21AnimalsBenzylaminesCell LineageChemokine CXCL12CyclamsEarEpidermal CellsEpidermisExtremitiesHeterocyclic CompoundsKeratinocytesLeukocytesMiceProtein TransportReceptors, CXCR4BenzylaminesChemokine CXCL12Cxcl12 protein, mouseCXCR4 protein, mouseCyclamsCyclin-Dependent Kinase Inhibitor p21Heterocyclic CompoundsplerixaforReceptors, CXCR4developmental biologygeneticsmolecular biologyregenerative medicinetissue regeneration

Identifiers

PMID26494786
PMCPMC4617975
OpenAlexW2112373120

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.