Evidence map›Paper›PMID 27141287›Full record

ArticleSkeletal muscle2016

Laminin and Matrix metalloproteinase 11 regulate Fibronectin levels in the zebrafish myotendinous junction.

Molly H Jenkins, Sarah S Alrowaished, Michelle F Goody, Bryan D Crawford, Clarissa A Henry

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026
    Review
  3. Article
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  11. Review
  12. NullInternational journal of molecular sciences · 2021
    Article
  13. Review
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  15. Review
  16. Article
  17. Article
  18. The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation.International journal of molecular sciences · 2018
    Article
  19. Article
  20. Matrix-metalloproteinases as targets for controlled delivery in cancer: An analysis of upregulation and expression.Journal of controlled release : official journal of the Controlled Release Society · 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

5 authors at 2 institutions in 2 countries.

Molly H JenkinsSchool of Biology and Ecology, University of Maine, 217 Hitchner Hall, Orono, ME 04469 USA.
Sarah S AlrowaishedSchool of Biology and Ecology, University of Maine, 217 Hitchner Hall, Orono, ME 04469 USA.
Michelle F GoodySchool of Biology and Ecology, University of Maine, 217 Hitchner Hall, Orono, ME 04469 USA.
Bryan D Crawford *Department of Biology, University of New Brunswick, Fredericton, NB Canada.
Clarissa A Henry *School of Biology and Ecology, University of Maine, 217 Hitchner Hall, Orono, ME 04469 USA.
University of Maine · USUniversity of New Brunswick · CA

Funding

Mechanisms underlying Paxillin-mediated amelioration of muscle degenerationR03HD077545 · NICHD · UNIVERSITY OF MAINE ORONO · PI HENRY, CLARISSA A · 2013 to 2014
$141k
NICHD NIH HHS 5R03HD077545NICHD NIH HHS R03 HD077545
6 · The paper itself

Abstract

backgroundRemodeling of the extracellular matrix (ECM) regulates cell adhesion as well as signaling between cells and their microenvironment. Despite the importance of tightly regulated ECM remodeling for normal muscle development and function, mechanisms underlying ECM remodeling in vivo remain elusive. One excellent paradigm in which to study ECM remodeling in vivo is morphogenesis of the myotendinous junction (MTJ) during zebrafish skeletal muscle development. During MTJ development, there are dramatic shifts in the primary components comprising the MTJ matrix. One such shift involves the replacement of Fibronectin (Fn)-rich matrix, which is essential for both somite and early muscle development, with laminin-rich matrix essential for normal function of the myotome. Here, we investigate the mechanism underlying this transition.

resultsWe show that laminin polymerization indirectly promotes Fn downregulation at the MTJ, via a matrix metalloproteinase 11 (Mmp11)-dependent mechanism. Laminin deposition and organization is required for localization of Mmp11 to the MTJ, where Mmp11 is both necessary and sufficient for Fn downregulation in vivo. Furthermore, reduction of residual Mmp11 in laminin mutants promotes a Fn-rich MTJ that partially rescues skeletal muscle architecture.

conclusionsThese results identify a mechanism for Fn downregulation at the MTJ, highlight crosstalk between laminin and Fn, and identify a new in vivo function for Mmp11. Taken together, our data demonstrate a novel signaling pathway mediating Fn downregulation. Our data revealing new regulatory mechanisms that guide ECM remodeling during morphogenesis in vivo may inform pathological conditions in which Fn is dysregulated.

Indexed as

Muscle DevelopmentAnimalsAnimals, Genetically ModifiedDown-RegulationFibronectinsGene Expression Regulation, DevelopmentalGenotypeLamininMatrix Metalloproteinase 11Muscle, SkeletalMutationPhenotypeSignal TransductionTendonsTime FactorsTissue Culture TechniquesFibronectinsLamininMatrix Metalloproteinase 11Zebrafish ProteinsFibronectinLamininMmp11Muscle developmentZebrafish

Identifiers

PMID27141287
PMCPMC4852425
OpenAlexW2339585327

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.