Evidence map›Paper›PMID 20855943›Full record

ArticleCell cycle (Georgetown, Tex.)2010

Epimorphic regeneration in mice is p53-independent.

L Matthew Arthur, Renee M Demarest, Lise Clark, Dmitri Gourevitch, Kamila Bedelbaeva, Rhonda Anderson, Andrew Snyder, Anthony J Capobianco, Paul Lieberman, Lionel Feigenbaum and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Prx1NPJ Regenerative medicine · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Improved biomechanical and biological outcomes in the MRL/MpJ murine strain following a full-length patellar tendon injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2015
    Article
  9. Article
  10. From Immunity and Vaccines to Mammalian Regeneration.The Journal of infectious diseases · 2015
    Article
  11. Review
  12. Article
  13. Tumor suppressors: enhancers or suppressors of regeneration?Development (Cambridge, England) · 2013
    Article
  14. The super super-healing MRL mouse strain.Frontiers in biology · 2012
    Article
  15. Review
  16. The role of p21 in regulating mammalian regeneration.Stem cell research & therapy · 2011
    Article
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

11 authors at 2 institutions in 1 country.

L Matthew ArthurThe Wistar Institute, Science Applications International Corporation-Frederick, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD, USA.
Renee M Demarest
Lise Clark
Dmitri Gourevitch
Kamila Bedelbaeva
Rhonda Anderson
Andrew Snyder
Anthony J Capobianco
Paul Lieberman
Lionel Feigenbaum
E Heber-Katz
The Wistar Institute · USUniversity of Miami · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
NCI NIH HHS 5T32CA09171NCI NIH HHS P30 CA010815NCI NIH HHS P30 CA10815NCI NIH HHS T32 CA009171
6 · The paper itself

Abstract

The process of regeneration is most readily studied in species of sponge, hydra, planarian and salamander (i.e., newt and axolotl). The closure of MRL mouse ear pinna through-and-through holes provides a mammalian model of unusual wound healing/regeneration in which a blastema-like structure closes the ear hole and cartilage and hair follicles are replaced. Recent studies, based on a broad level of DNA damage and a cell cycle pattern of G₂/M "arrest," showed that p21(Cip1/Waf1) was missing from the MRL mouse ear and that a p21-null mouse could close its ear holes. Given the p53/p21 axis of control of DNA damage, cell cycle arrest, apoptosis and senescence, we tested the role of p53 in the ear hole regenerative response. Using backcross mice, we found that loss of p53 in MRL mice did not show reduced healing. Furthermore, cross sections of MRL. p53(-/-) mouse ears at 6 weeks post-injury showed an increased level of adipocytes and chondrocytes in the region of healing whereas MRL or p21(-/-) mice showed chondrogenesis alone in this same region, though at later time points. In addition, we also investigated other cell cycle-related mutant mice to determine how p21 was being regulated. We demonstrate that p16 and Gadd45 null mice show little healing capacity. Interestingly, a partial healing phenotype in mice with a dual Tgfβ/Rag2 knockout mutation was seen. These data demonstrate an independence of p53 signaling for mouse appendage regeneration and suggest that the role of p21 in this process is possibly through the abrogation of the Tgfβ/Smad pathway.

Indexed as

RegenerationAnimalsCell DifferentiationCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsEarMiceMice, KnockoutSignal TransductionSmad ProteinsTransforming Growth Factor betaTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsRag2 protein, mouseSmad ProteinsTransforming Growth Factor betaTumor Suppressor Protein p53

Identifiers

PMID20855943
PMCPMC3047795
OpenAlexW2047593912

What OpenQuestion holds

Textmetadata
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.