Evidence map›Paper›PMID 26970186›Full record

ArticleCellular signalling2016

Common pathways regulate Type III TGFβ receptor-dependent cell invasion in epicardial and endocardial cells.

Cynthia R Clark, Jamille Y Robinson, Nora S Sanchez, Todd A Townsend, Julian A Arrieta, W David Merryman, David Z Trykall, Harold E Olivey, Charles C Hong, Joey V Barnett

Abstract read
In one paragraph

Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Loss ofLife (Basel, Switzerland) · 2025
    Article
  2. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
    Review
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  8. Article
  9. MicroRNA let-7a regulates angiogenesis by targeting TGFBR3 mRNA.Journal of cellular and molecular medicine · 2019
    Article
  10. Review
  11. 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

10 authors at 3 institutions in 1 country.

Cynthia R ClarkDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: cynthia.r.allison@vanderbilt.edu.
Jamille Y RobinsonDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: jamille.robinson@vanderbilt.edu.
Nora S SanchezDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: NSSanchez@mdanderson.org.
Todd A TownsendDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: ttownsend@genetics.utah.edu.
Julian A ArrietaDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: julian.a.arrieta@Vanderbilt.edu.
W David MerrymanDept. of Biomedical Engineering, Vanderbilt University, Nashville, TN 37212. Electronic address: david.merryman@vanderbilt.edu.
David Z TrykallDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: david.trykall@vanderbilt.edu.
Harold E OliveyDept. of Biology, Indiana University-Northwest, Gary, IN 46408, United States. Electronic address: holivey@iun.edu.
Charles C HongDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, United States; Research Medicine, Veterans Affairs TVHS, Nashville, TN 37212, United States. Electronic address: charles.c.hong@vanderbilt.edu.
Joey V BarnettDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, United States; Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, United States. Electronic address: joey.barnett@vanderbilt.edu.
Vanderbilt University · USIndiana University Northwest · USVA Tennessee Valley Healthcare System · US

Funding

Understanding and preventing HLA-associated drug reactionsP50GM115305 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PHILLIPS, ELIZABETH, RODEN, DAN M · 2015 to 2019
$13.0M
Vanderbilt/Meharry Initiative for Minority Student DvptR25GM062459 · NIGMS · VANDERBILT UNIVERSITY · PI VELEZ EDWARDS, DIGNA R · 2002 to 2020
$10.4M
SysCODE Heart Valve Design and EngineeringRL1HL092551 · NHLBI · VANDERBILT UNIVERSITY · PI BALDWIN, H SCOTT · 2007 to 2011
$2.8M
Type III Transforming Growth Factor beta Receptor in Coronary Vessel DevelopmentR01HL085708 · NHLBI · VANDERBILT UNIVERSITY · PI BARNETT, JOEY VICTOR · 2008 to 2011
$1.7M
Short Term Training for Minority StudentsR25HL096223 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI JOYCE, SEBASTIAN · 2009 to 2020
$841k
NHLBI NIH HHS HL085708NHLBI NIH HHS R01 HL085708NHLBI NIH HHS R25 HL096223NHLBI NIH HHS R25 HL96223NHLBI NIH HHS RL1 HL092551NIGMS NIH HHS GM062459NIGMS NIH HHS P50 GM115305NIGMS NIH HHS R25 GM062459PHS HHS U54 092551
6 · The paper itself

Abstract

Epithelial-Mesenchymal Transformation (EMT) and the subsequent invasion of epicardial and endocardial cells during cardiac development is critical to the development of the coronary vessels and heart valves. The transformed cells give rise to cardiac fibroblasts and vascular smooth muscle cells or valvular interstitial cells, respectively. The Type III Transforming Growth Factor β (TGFβR3) receptor regulates EMT and cell invasion in both cell types, but the signaling mechanisms downstream of TGFβR3 are not well understood. Here we use epicardial and endocardial cells in in vitro cell invasion assays to identify common mechanisms downstream of TGFβR3 that regulate cell invasion. Inhibition of NF-κB activity blocked cell invasion in epicardial and endocardial cells. NF-κB signaling was found to be dysregulated in Tgfbr3(-/-) epicardial cells which also show impaired cell invasion in response to ligand. TGFβR3-dependent cell invasion is also dependent upon Activin Receptor-Like Kinase (ALK) 2, ALK3, and ALK5 activity. A TGFβR3 mutant that contains a threonine to alanine substitution at residue 841 (TGFβR3-T841A) induces ligand-independent cell invasion in both epicardial and endocardial cells in vitro. These findings reveal a role for NF-κB signaling in the regulation of epicardial and endocardial cell invasion and identify a mutation in TGFβR3 which stimulates ligand-independent signaling.

Indexed as

Cell MovementEpithelial-Mesenchymal TransitionSignal TransductionActivin ReceptorsAnimalsCell LineEndocardiumMiceMutationNF-kappa BPericardiumReceptors, Transforming Growth Factor betaActivin ReceptorsNF-kappa BReceptors, Transforming Growth Factor betaBone morphogenic proteinEndocardial cellEpicardial cellInvasionNuclear factor-kappa BTransforming Growth Factor Beta

Identifiers

PMID26970186
PMCPMC4827451
OpenAlexW2294201550

What OpenQuestion holds

Textmetadata
LicenceTDM
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.