Evidence map›Paper›PMID 24016759›Full record

ArticleDevelopmental biology2013

Tbx18 regulates development of the epicardium and coronary vessels.

San-Pin Wu, Xiu-Rong Dong, Jenna N Regan, Chang Su, Mark W Majesky

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

66 citing papers in PubMed, 108 citations in OpenAlex.

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  10. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
    Review
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6 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

San-Pin WuDepartment of Molecular & Cellular Biology, Baylor College of Medicine, Houston, TX 77030, United States. Electronic address: sanpinw@bcm.edu.
Xiu-Rong Dong
Jenna N Regan
Chang Su
Mark W Majesky
Baylor College of Medicine · USUniversity of North Texas · USUniversity of Washington · USWashington University in St. Louis · US

Funding

THE CONTRACTILE SYSTEM OF VASCULAR SMOOTH MUSCLEP01HL019242 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI OWENS, GARY K · 1985 to 2009
$16.9M
NRSA IN GENETICST32GM007092 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SEKELSKY, JEFF J. · 1985 to 2019
$5.9M
Hedgehog Signaling in the AdventitiaR01HL093594 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAJESKY, MARK W. · 2009 to 2012
$1.8M
CARDIOVASCULAR SCIENCES TRAINING GRANTT32HL007816 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI BURNS, ALAN R · 1996 to 2005
$1.4M
NHLBI NIH HHS HL-07816NHLBI NIH HHS HL-19242NHLBI NIH HHS HL-93594NHLBI NIH HHS P01 HL019242NHLBI NIH HHS R01 HL093594NHLBI NIH HHS T32 HL007816NIGMS NIH HHS T32 GM007092
6 · The paper itself

Abstract

The epicardium and coronary vessels originate from progenitor cells in the proepicardium. Here we show that Tbx18, a T-box family member highly expressed in the proepicardium, controls critical early steps in coronary development. In Tbx18(-/-) mouse embryos, both the epicardium and coronary vessels exhibit structural and functional defects. At E12.5, the Tbx18-deficient epicardium contains protrusions and cyst-like structures overlying a disorganized coronary vascular plexus that contains ectopic structures resembling blood islands. At E13.5, the left and right coronary stems form correctly in mutant hearts. However, analysis of PECAM-1 whole mount immunostaining, distribution of SM22α(lacZ/+) activity, and analysis of coronary vascular casts suggest that defective vascular plexus remodeling produces a compromised arterial network at birth consisting of fewer distributing conduit arteries with smaller lumens and a reduced capacity to conduct blood flow. Gene expression profiles of Tbx18(-/-) hearts at E12.5 reveal altered expression of 79 genes that are associated with development of the vascular system including sonic hedgehog signaling components patched and smoothened, VEGF-A, angiopoietin-1, endoglin, and Wnt factors compared to wild type hearts. Thus, formation of coronary vasculature is responsive to Tbx18-dependent gene targets in the epicardium, and a poorly structured network of coronary conduit vessels is formed in Tbx18 null hearts due to defects in epicardial cell signaling and fate during heart development. Lastly, we demonstrate that Tbx18 possesses a SRF/CArG box dependent repressor activity capable of inhibiting progenitor cell differentiation into smooth muscle cells, suggesting a potential function of Tbx18 in maintaining the progenitor status of epicardial-derived cells.

Indexed as

AnimalsAnimals, Newbornbeta-GalactosidaseCell DifferentiationCoronary CirculationCoronary VesselsEmbryo, MammalianGene Expression ProfilingGene Expression Regulation, DevelopmentalMiceMyocytes, Smooth MusclePericardiumRepressor ProteinsSerum Response FactorT-Box Domain ProteinsTranscription, Geneticbeta-GalactosidaseRepressor ProteinsSerum Response FactorT-Box Domain ProteinsTbx18 protein, mouseCardiac developmentCoronary circulationEpicardiumHedgehog signalingT-box 18

Identifiers

PMID24016759
PMCPMC4172450
OpenAlexW1994117018

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.