Evidence map›Paper›PMID 21920357›Full record

ArticleDevelopmental biology2011

Mmp15 is a direct target of Snai1 during endothelial to mesenchymal transformation and endocardial cushion development.

Ge Tao, Agata K Levay, Thomas Gridley, Joy Lincoln

Abstract read
In one paragraph

Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. mCell & bioscience · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. A coherent FOXO3-SNAI2 feed-forward loop in autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Article
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  13. Article
  14. The Mesenchymal Cap of the Atrial Septum and Atrial and Atrioventricular Septation.Journal of cardiovascular development and disease · 2020
    Review
  15. Article
  16. Breaking down barriers: the evolution of cell invasion.Current opinion in genetics & development · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Ge TaoDepartment of Molecular and Cellular Pharmacology, Leonard M. Miller School of Medicine, University of Miami, Florida 33101, USA.
Agata K Levay
Thomas Gridley
Joy Lincoln
University of Miami · USMaine Medical Center · US

Funding

GENETIC CONTROL OF MESODERM AND NEURAL CREST FORMATIONR01HD034883 · NICHD · MAINEHEALTH · PI GRIDLEY, THOMAS HOOKER · 1998 to 2012
$4.4M
Molecular regulation of heart valve development and function.R01HL091878 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LINCOLN, JOY · 2008 to 2012
$2.2M
NHLBI NIH HHS 1R01HL091878-JLNHLBI NIH HHS R01 HL091878NICHD NIH HHS HD034883-TGNICHD NIH HHS R01 HD034883
6 · The paper itself

Abstract

Cardiac valves originate from endocardial cushions (EC) formed by endothelial-to-mesenchymal transformation (EMT) during embryogenesis. The zinc-finger transcription factor Snai1 has previously been reported to be important for EMT during organogenesis, yet its role in early valve development has not been directly examined. In this study we show that Snai1 is highly expressed in endothelial, and newly transformed mesenchyme cells during EC development. Mice with targeted snai1 knockdown display hypocellular ECs at E10.5 associated with decreased expression of mesenchyme cell markers and downregulation of the matrix metalloproteinase (mmp) family member, mmp15. Snai1 overexpression studies in atrioventricular canal collagen I gel explants indicate that Snai1 is sufficient to promote mmp15 expression, cell transformation, and mesenchymal cell migration and invasion. However, treatment with the catalytically active form of MMP15 promotes cell motility, and not transformation. Further, we show that Snai1-mediated cell migration requires MMP activity, and caMMP15 treatment rescues attenuated migration defects observed in murine ECs following snai1 knockdown. Together, findings from this study reveal previously unappreciated mechanisms of Snai1 for the direct regulation of MMPs during EC development.

Indexed as

AnimalsBinding SitesCell MovementCells, CulturedChick EmbryoChlorocebus aethiopsCOS CellsDipeptidesEndocardial CushionsEndotheliumFemaleGene Expression Regulation, DevelopmentalHeart ValvesImmunohistochemistryMaleMatrix Metalloproteinase 15DipeptidesMatrix Metalloproteinase 15Matrix Metalloproteinase InhibitorsMmp15 protein, mouseN-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamideProtease InhibitorsSnai1 protein, mouseSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID21920357
PMCPMC3202673
OpenAlexW1983738631

What OpenQuestion holds

Textmetadata
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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.