Evidence map›Paper›PMID 17250821›Full record

ArticleDevelopmental biology2007

Endoglin and Alk5 regulate epithelial-mesenchymal transformation during cardiac valve formation.

Melania E Mercado-Pimentel, Antony D Hubbard, Raymond B Runyan

Open access · greenAbstract readComparative Study
In one paragraph

Article in Developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
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  5. Article
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  8. Review
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  11. Runx2-I is an Early Regulator of Epithelial-Mesenchymal Cell Transition in the Chick Embryo.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  12. Article
  13. Article
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  15. Article
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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

3 authors at 1 institution in 1 country.

Melania E Mercado-PimentelDepartment of Cell Biology and Anatomy, University of Arizona, 1501 N. Campbell Ave., P.O. Box 245044, Tucson, AZ 85724-5044, USA.
Antony D Hubbard
Raymond B Runyan
University of Arizona · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI Paloma Inés Beamer · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
Regulation of cell transformationP01HL063926 · NHLBI · UNIVERSITY OF ARIZONA · PI RUNYAN, RAYMOND BRUCE · 2000 to 2004
$8.9M
NHLBI NIH HHS HL63926NHLBI NIH HHS P01 HL063926NIEHS NIH HHS ES007091NIEHS NIH HHS ES06694NIEHS NIH HHS P30 ES006694NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

Endoglin is an accessory receptor for TGFbeta and can associate with Alk5 or Alk2. Although prior studies indicated that endoglin and Alk5 were not directly involved in epithelial-mesenchymal transformation (EMT) in the heart, the expression pattern of endoglin prompted a re-examination. We here show that loss of endoglin expression mediated by either antisense DNA or siRNA results in a direct perturbation of EMT and reduced expression of EMT markers including slug, runx2, RhoA, and latrophilin-2. An examination of BrdU incorporation shows that, while endoglin regulates proliferation at an early stage, reduced endothelial cell proliferation does not account for the loss of mesenchyme. As Alk5 interacts with endoglin, we utilized siRNA and a specific inhibitor, HTS466284 (HTS), to perturb this receptor as well. Alk5 inhibition produced similar effects to the inhibition of endoglin. There was a reduction in mesenchymal cell formation and loss of EMT marker expression similar to that seen with endoglin. Alk5 kinase inhibition produced a similar loss of EMT marker expression but showed a contrasting upregulation of the proliferation and remodeling markers, Cyclin B2 and beta-catenin. Alk5 and endoglin both mediate endothelial cell proliferation in younger explants but, by stage 16, loss of endoglin no longer alters proliferation rates. These data show that both Alk5 and endoglin are directly involved in the process of EMT, that they interact with both TGFbeta-regulated activation and invasion pathways and that the roles of these receptors change during cardiac development.

Indexed as

AnimalsBromodeoxyuridineCell DifferentiationChick EmbryoDNA PrimersEpithelial CellsGene Expression Regulation, DevelopmentalHeart ValvesIn Situ HybridizationMesodermReceptors, Transforming Growth Factor betaReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingBromodeoxyuridineDNA PrimersReceptors, Transforming Growth Factor betaRNA, Small Interfering

Identifiers

PMID17250821
PMCPMC2001167
OpenAlexW2092350154

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.