Evidence map›Paper›PMID 38376371›Full record

ArticleeLife2024

Spatial-temporal order-disorder transition in angiogenic NOTCH signaling controls cell fate specification.

Tae-Yun Kang, Federico Bocci, Qing Nie, José N Onuchic, Andre Levchenko

Open access · goldAbstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. YAP/TAZ drives Notch and angiogenesis mechanoregulation in silico.NPJ systems biology and applications · 2024
    Article
  7. Article
  8. Theoretical and computational tools to model multistable gene regulatory networks.Reports on progress in physics. Physical Society (Great Britain) · 2023
    Review
  9. 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

5 authors at 3 institutions in 2 countries.

Tae-Yun Kang *Department of Biomedical Engineering, Yale University, New Haven, United States.ORCID https://orcid.org/0000-0002-6122-0870
Federico Bocci *NSF-Simons Center for Multiscale Cell Fate Research, University of California Irvine, Irvine, United States.ORCID https://orcid.org/0000-0003-4302-9906
Qing NieNSF-Simons Center for Multiscale Cell Fate Research, University of California Irvine, Irvine, United States.ORCID https://orcid.org/0000-0002-8804-3368
José N OnuchicCenter for Theoretical Biological Physics, Rice University, Houston, United States.ORCID https://orcid.org/0000-0002-9448-0388
Andre LevchenkoDepartment of Biomedical Engineering, Yale University, New Haven, United States.ORCID https://orcid.org/0000-0001-6262-1222
University of California, Irvine · USYale University · USCenter for Theoretical Biological Physics · US

Funding

Systems analysis of phenotypic switch in control of cancer invasionU54CA209992 · NCI · YALE UNIVERSITY · PI LEVCHENKO, ANDRE · 2016 to 2021
$10.1M
NCI NIH HHS U54 CA209992NIH HHS NCI U54 CA209992
6 · The paper itself

Abstract

Angiogenesis is a morphogenic process resulting in the formation of new blood vessels from pre-existing ones, usually in hypoxic micro-environments. The initial steps of angiogenesis depend on robust differentiation of oligopotent endothelial cells into the Tip and Stalk phenotypic cell fates, controlled by NOTCH-dependent cell-cell communication. The dynamics of spatial patterning of this cell fate specification are only partially understood. Here, by combining a controlled experimental angiogenesis model with mathematical and computational analyses, we find that the regular spatial Tip-Stalk cell patterning can undergo an order-disorder transition at a relatively high input level of a pro-angiogenic factor VEGF. The resulting differentiation is robust but temporally unstable for most cells, with only a subset of presumptive Tip cells leading sprout extensions. We further find that sprouts form in a manner maximizing their mutual distance, consistent with a Turing-like model that may depend on local enrichment and depletion of fibronectin. Together, our data suggest that NOTCH signaling mediates a robust way of cell differentiation enabling but not instructing subsequent steps in angiogenic morphogenesis, which may require additional cues and self-organization mechanisms. This analysis can assist in further understanding of cell plasticity underlying angiogenesis and other complex morphogenic processes.

Indexed as

Endothelial CellsSignal TransductionCell CommunicationCell DifferentiationMorphogenesisangiogenesiscomputational biologyhumanNOTCH signalingorder–disorder transitionsystems biologyTip–Stalk fateTuring pattern

Identifiers

PMID38376371
PMCPMC10942579
OpenAlexW4385719279

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.