Evidence map›Paper›PMID 19700622›Full record

ArticleDevelopment (Cambridge, England)2009

Connexin 43 regulates epicardial cell polarity and migration in coronary vascular development.

David Y Rhee, Xiao-Qing Zhao, Richard J B Francis, Guo Ying Huang, John D Mably, Cecilia W Lo

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  11. Two genetic variants inFrontiers in cardiovascular medicine · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Muscularization of the Mesenchymal Outlet Septum during Cardiac Development.Journal of cardiovascular development and disease · 2020
    Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

David Y RheeLaboratory of Developmental Biology, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Xiao-Qing Zhao
Richard J B Francis
Guo Ying Huang
John D Mably
Cecilia W Lo
Boston Children's Hospital · US

Funding

Molecular, Cellular, & Developmental Dynamics PhD ProgramT32GM007226 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI VAN VACTOR, DAVID L. · 1985 to 2021
$14.4M
Cell-cell Interactions /Cell Signaling In CardiovascularZ01HL005701 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LO, CECILIA W. · 2002 to 2008
$6.2M
Cell and Molecular Basis for Congenital Heart DiseaseZIAHL005701 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LO, CECILIA W. · 2009 to 2010
$3.9M
NHLBI NIH HHS ZO1-HL005701NIGMS NIH HHS T32 GM007226
6 · The paper itself

Abstract

Connexin 43 knockout (Cx43 KO) mice exhibit conotruncal malformations and coronary artery defects. We observed epicardial blisters in the Cx43 KO hearts that suggest defects in epicardial epithelial-mesenchymal transformation (EMT), a process that generates coronary vascular progenitors. Analysis using a three-dimensional collagen gel invasion assay showed that Cx43 KO epicardial cells are less invasive and that, unlike wild-type epicardial cells, they fail to organize into thin vessel-like projections. Examination of Cx43 KO hearts using Wt1 as an epicardial marker revealed a disorganized pattern of epicardial cell infiltration. Time-lapse imaging and motion analysis using epicardial explants showed a defect in directional cell migration. This was associated with changes in the actin/tubulin cytoskeleton. A defect in cell polarity was indicated by a failure of the microtubule-organizing center to align with the direction of cell migration. Forced expression of Cx43 constructs in epicardial explants showed the Cx43 tubulin-binding domain is required for Cx43 modulation of cell polarity and cell motility. Pecam staining revealed early defects in remodeling of the primitive coronary vascular plexuses in the Cx43 KO heart. Together, these findings suggest an early defect in coronary vascular development arising from a global perturbation of the cytoarchitecture of the cell. Consistent with this, we found aberrant myocardialization of the outflow tract, a process also known to be EMT dependent. Together, these findings suggest cardiac defects in the Cx43 KO mice arise from the disruption of cell polarity, a process that may be dependent on Cx43-tubulin interactions.

Indexed as

Cell PolarityCoronary VesselsMyocardiumAnimalsCell MovementCells, CulturedConnexin 43CytoskeletonHeartMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutPhosphoproteinsZonula Occludens-1 ProteinConnexin 43Membrane ProteinsPhosphoproteinsTjp1 protein, mouseZonula Occludens-1 Protein

Identifiers

PMID19700622
PMCPMC2730372
OpenAlexW2147917329

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.