Evidence map›Paper›PMID 27138650›Full record

ArticleNature communications2016

Laminin regulates PDGFRβ(+) cell stemness and muscle development.

Yao Yao, Erin H Norris, Christopher E Mason, Sidney Strickland

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Cell-Instructive Biomaterials with Native-Like Biochemical Complexity.Annual review of biomedical engineering · 2025
    Review
  5. Article
  6. MuSCs and IPCs: roles in skeletal muscle homeostasis, aging and injury.Cellular and molecular life sciences : CMLS · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Basement membrane and blood-brain barrier.Stroke and vascular neurology · 2019
    Review
  15. Review
  16. Pericytes in Muscular Dystrophies.Advances in experimental medicine and biology · 2019
    Article
  17. Fat fibrosis: friend or foe?JCI insight · 2018
    Review
  18. Article
  19. Isolation of Type I and Type II Pericytes from Mouse Skeletal Muscles.Journal of visualized experiments : JoVE · 2017
    Article
  20. Laminin: loss-of-function studies.Cellular and molecular life sciences : CMLS · 2017
    Review
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

4 authors at 2 institutions in 1 country.

Yao YaoLaboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA.
Erin H NorrisLaboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA.
Christopher E MasonDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, New York 10065, USA.
Sidney StricklandLaboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA.
Rockefeller University · USCornell University · US

Funding

Role of the tPA/plasmin System in Alzheimers DiseaseR01NS050537 · NINDS · ROCKEFELLER UNIVERSITY · PI STRICKLAND, SIDNEY · 2004 to 2015
$5.7M
NINDS NIH HHS NS050537NINDS NIH HHS R01 NS050537
6 · The paper itself

Abstract

Muscle-resident PDGFRβ(+) cells, which include pericytes and PW1(+) interstitial cells (PICs), play a dual role in muscular dystrophy. They can either undergo myogenesis to promote muscle regeneration or differentiate into adipocytes and other cells to compromise regeneration. How the differentiation and fate determination of PDGFRβ(+) cells are regulated, however, remains unclear. Here, by utilizing a conditional knockout mouse line, we report that PDGFRβ(+) cell-derived laminin inhibits their proliferation and adipogenesis, but is indispensable for their myogenesis. In addition, we show that laminin alone is able to partially reverse the muscle dystrophic phenotype in these mice at the molecular, structural and functional levels. Further RNAseq analysis reveals that laminin regulates PDGFRβ(+) cell differentiation/fate determination via gpihbp1. These data support a critical role of laminin in the regulation of PDGFRβ(+) cell stemness, identify an innovative target for future drug development and may provide an effective treatment for muscular dystrophy.

Indexed as

AdipocytesAdipogenesisAnimalsCell DifferentiationCell ProliferationGene Expression RegulationLamininMiceMice, KnockoutMuscle CellsMuscle DevelopmentMuscle, SkeletalMuscular DystrophiesPericytesReceptor, Platelet-Derived Growth Factor betaReceptors, LipoproteinGPI-HBP1 protein, mouseLamininReceptor, Platelet-Derived Growth Factor betaReceptors, Lipoprotein

Identifiers

PMID27138650
PMCPMC4857399
OpenAlexW2345664705

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.