Evidence map›Paper›PMID 21124733›Full record

ArticlePloS one2010

Dlk1 is necessary for proper skeletal muscle development and regeneration.

Jolena N Waddell, Peijing Zhang, Yefei Wen, Sanjay K Gupta, Aleksey Yevtodiyenko, Jennifer V Schmidt, Christopher A Bidwell, Ashok Kumar, Shihuan Kuang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

71 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
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  14. Review
  15. Functional Identification of PorcineAnimals : an open access journal from MDPI · 2022
    Article
  16. Review
  17. Emerging Roles of DLK1 in the Stem Cell Niche and Cancer Stemness.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022
    Review
  18. Fennel (Heliyon · 2021
    Article
  19. Review
  20. Article

11 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

9 authors at 4 institutions in 1 country.

Jolena N WaddellDepartment of Animal Sciences, Purdue University, West Lafayette, Indiana, USA.
Peijing Zhang
Yefei Wen
Sanjay K Gupta
Aleksey Yevtodiyenko
Jennifer V Schmidt
Christopher A Bidwell
Ashok Kumar
Shihuan Kuang
Purdue University West Lafayette · USUniversity of Louisville · USStanford University · USUniversity of Illinois Chicago · US

Funding

Notch Regulation of Stem Cell Fate in MuscleR01AR060652 · NIAMS · PURDUE UNIVERSITY · PI KUANG, SHIHUAN · 2010 to 2014
$1.6M
An Imprinted Gene Cluster on Mouse Chromosome 12R01HD042013 · NICHD · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SCHMIDT, JENNIFER V · 2004 to 2008
$1.3M
NIAMS NIH HHS 1R01AR060652-01A1NIAMS NIH HHS R01 AR060652NICHD NIH HHS HD042013NICHD NIH HHS R01 HD042013
6 · The paper itself

Abstract

Delta-like 1homolog (Dlk1) is an imprinted gene encoding a transmembrane protein whose increased expression has been associated with muscle hypertrophy in animal models. However, the mechanisms by which Dlk1 regulates skeletal muscle plasticity remain unknown. Here we combine conditional gene knockout and over-expression analyses to investigate the role of Dlk1 in mouse muscle development, regeneration and myogenic stem cells (satellite cells). Genetic ablation of Dlk1 in the myogenic lineage resulted in reduced body weight and skeletal muscle mass due to reductions in myofiber numbers and myosin heavy chain IIB gene expression. In addition, muscle-specific Dlk1 ablation led to postnatal growth retardation and impaired muscle regeneration, associated with augmented myogenic inhibitory signaling mediated by NF-κB and inflammatory cytokines. To examine the role of Dlk1 in satellite cells, we analyzed the proliferation, self-renewal and differentiation of satellite cells cultured on their native host myofibers. We showed that ablation of Dlk1 inhibits the expression of the myogenic regulatory transcription factor MyoD, and facilitated the self-renewal of activated satellite cells. Conversely, Dlk1 over-expression inhibited the proliferation and enhanced differentiation of cultured myoblasts. As Dlk1 is expressed at low levels in satellite cells but its expression rapidly increases upon myogenic differentiation in vitro and in regenerating muscles in vivo, our results suggest a model in which Dlk1 expressed by nascent or regenerating myofibers non-cell autonomously promotes the differentiation of their neighbor satellite cells and therefore leads to muscle hypertrophy.

Indexed as

RegenerationAnimalsBlotting, WesternCalcium-Binding ProteinsCell DifferentiationCell LineCell ProliferationCells, CulturedImmunohistochemistryIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutMuscle Fibers, SkeletalMuscle, SkeletalMyoblastsCalcium-Binding ProteinsDlk1 protein, mouseIntercellular Signaling Peptides and ProteinsMyoD1 myogenic differentiation proteinMyoD Protein

Identifiers

PMID21124733
PMCPMC2993959
OpenAlexW2021037171

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.