Evidence map›Paper›PMID 17720695›Full record

ArticleDevelopment (Cambridge, England)2007

Vascular remodeling of the mouse yolk sac requires hemodynamic force.

Jennifer L Lucitti, Elizabeth A V Jones, Chengqun Huang, Ju Chen, Scott E Fraser, Mary E Dickinson

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 275 papers.

0numbers the graph read from it
0cells of the map it votes in
275citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

275 citing papers in PubMed, 488 citations in OpenAlex.

  1. Mechanics and mechanobiology of arterial development.Biomechanics and modeling in mechanobiology · 2026
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  13. The dynamics of tubulogenesis in development and disease.Development (Cambridge, England) · 2025
    Review
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  20. Article

215 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

6 authors at 1 institution in 1 country.

Jennifer L LucittiDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030, USA.
Elizabeth A V Jones
Chengqun Huang
Ju Chen
Scott E Fraser
Mary E Dickinson
California Institute of Technology · US

Funding

Molecular Physiology of the Cardiovascular SystemT32HL007676 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI HAMILTON, SUSAN L · 1989 to 2020
$7.9M
Imaging fluid forces in mouse cardiovascular developmentR01HL077187 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI DICKINSON, MARY E · 2005 to 2007
$1.1M
NHLBI NIH HHS R01 HL077187NHLBI NIH HHS R01 HL HL077187NHLBI NIH HHS T32 HL007676NHLBI NIH HHS T32 HL7676
6 · The paper itself

Abstract

The embryonic heart and vessels are dynamic and form and remodel while functional. Much has been learned about the genetic mechanisms underlying the development of the cardiovascular system, but we are just beginning to understand how changes in heart and vessel structure are influenced by hemodynamic forces such as shear stress. Recent work has shown that vessel remodeling in the mouse yolk sac is secondarily effected when cardiac function is reduced or absent. These findings indicate that proper circulation is required for vessel remodeling, but have not defined whether the role of circulation is to provide mechanical cues, to deliver oxygen or to circulate signaling molecules. Here, we used time-lapse confocal microscopy to determine the role of fluid-derived forces in vessel remodeling in the developing murine yolk sac. Novel methods were used to characterize flows in normal embryos and in embryos with impaired contractility (Mlc2a(-/-)). We found abnormal plasma and erythroblast circulation in these embryos, which led us to hypothesize that the entry of erythroblasts into circulation is a key event in triggering vessel remodeling. We tested this by sequestering erythroblasts in the blood islands, thereby lowering the hematocrit and reducing shear stress, and found that vessel remodeling and the expression of eNOS (Nos3) depends on erythroblast flow. Further, we rescued remodeling defects and eNOS expression in low-hematocrit embryos by restoring the viscosity of the blood. These data show that hemodynamic force is necessary and sufficient to induce vessel remodeling in the mammalian yolk sac.

Indexed as

Blood CirculationEmbryonic DevelopmentAnimalsBlood VesselsBlood ViscosityEmbryo, MammalianErythroblastsHematocritMiceMice, Mutant StrainsMicroscopy, ConfocalMyosin Light ChainsNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIShear StrengthYolk SacMlc2a protein, mouseMyosin Light ChainsNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos3 protein, mouse

Identifiers

PMID17720695
PMCPMC4260474
OpenAlexW2125332169

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.