Evidence map›Paper›PMID 19710169›Full record

ArticleDevelopment (Cambridge, England)2009

Spatial and temporal regulation of coronary vessel formation by calcineurin-NFAT signaling.

Miriam Zeini, Calvin T Hang, Joshua Lehrer-Graiwer, Tiffany Dao, Bin Zhou, Ching-Pin Chang

Open access · bronzeAbstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. CCBE1 in Cardiac Development and Disease.Frontiers in genetics · 2022
    Review
  6. Article
  7. Article
  8. The Endocardium and Heart Valves.Cold Spring Harbor perspectives in biology · 2020
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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.

Miriam ZeiniDivision of Cardiovascular Medicine, Department of Medicine, Stanford University, Stanford, CA 94305, USA.
Calvin T Hang
Joshua Lehrer-Graiwer
Tiffany Dao
Bin Zhou
Ching-Pin Chang
Stanford University · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Mechanisms of Nural Crest Cell DevelopmentR01HL085345 · NHLBI · STANFORD UNIVERSITY · PI CHANG, CHING-PIN · 2006 to 2010
$2.3M
TRANSCRIPTIONAL REGULATION OF ENDOCARDIAL DEVELOPMENTR01HL078881 · NHLBI · VANDERBILT UNIVERSITY · PI ZHOU, BIN · 2006 to 2010
$2.0M
VASCULAR BIOLOGY AND MEDICINE TRAININGT32HL007708 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 1992 to 2007
$1.9M
NCI NIH HHS 5T32 CA09302NCI NIH HHS T32 CA009302NHLBI NIH HHS HL078881NHLBI NIH HHS HL085345NHLBI NIH HHS R01 HL085345NHLBI NIH HHS T32 HL007708
6 · The paper itself

Abstract

Formation of the coronary vasculature requires reciprocal signaling between endothelial, epicardially derived smooth muscle and underlying myocardial cells. Our studies show that calcineurin-NFAT signaling functions in endothelial cells within specific time windows to regulate coronary vessel development. Mouse embryos exposed to cyclosporin A (CsA), which inhibits calcineurin phosphatase activity, failed to develop normal coronary vasculature. To determine the cellular site at which calcineurin functions for coronary angiogenesis, we deleted calcineurin in endothelial, epicardial and myocardial cells. Disruption of calcineurin-NFAT signaling in endothelial cells resulted in the failure of coronary angiogenesis, recapitulating the coronary phenotype observed in CsA-treated embryos. By contrast, deletion of calcineurin in either epicardial or myocardial cells had no effect on coronary vasculature during early embryogenesis. To define the temporal requirement for NFAT signaling, we treated developing embryos with CsA at overlapping windows from E9.5 to E12.5 and examined coronary development at E12.5. These experiments demonstrated that calcineurin-NFAT signaling functions between E10.5 and E11.5 to regulate coronary angiogenesis. Consistent with these in vivo observations, endothelial cells exposed to CsA within specific time windows in tissue culture were unable to form tubular structures and their cellular responses to VEGF-A were blunted. Thus, our studies demonstrate specific temporal and spatial requirements of NFAT signaling for coronary vessel angiogenesis. These requirements are distinct from the roles of NFAT signaling in the angiogenesis of peripheral somatic vessels, providing an example of the environmental influence of different vascular beds on the in vivo endothelial responses to angiogenic stimuli.

Indexed as

AnimalsBase SequenceBody PatterningCalcineurinCalcineurin InhibitorsCell DifferentiationCells, CulturedCoronary VesselsCyclosporineDNA PrimersEndothelial CellsHumansIn Vitro TechniquesMiceMice, Mutant StrainsMice, TransgenicCalcineurinCalcineurin InhibitorsCyclosporineDNA PrimersNFATC Transcription Factors

Identifiers

PMID19710169
PMCPMC2739147
OpenAlexW2142169340

What OpenQuestion holds

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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.