Evidence map›Paper›PMID 26943318›Full record

ArticleCell death and differentiation2016

Endothelial cell survival during angiogenesis requires the pro-survival protein MCL1.

E C Watson, L Whitehead, R H Adams, G Dewson, L Coultas

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
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  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Contribution of cell death signaling to blood vessel formation.Cellular and molecular life sciences : CMLS · 2021
    Review
  15. Physiological Functions of Mcl-1: Insights From Genetic Mouse Models.Frontiers in cell and developmental biology · 2021
    Review
  16. Article
  17. Article
  18. DeregulatedCells · 2019
    Article
  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

5 authors at 2 institutions in 2 countries.

E C WatsonDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC, Australia.
L WhiteheadDepartment of Medical Biology, University of Melbourne, 1G Royal Parade, VIC, Australia.ORCID 0000-0002-4388-9642
R H AdamsDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, Münster D, Germany.
G DewsonDepartment of Medical Biology, University of Melbourne, 1G Royal Parade, VIC, Australia.
L CoultasDevelopment and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC, Australia.
The University of Melbourne · AUUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is essential to match the size of blood vessel networks to the metabolic demands of growing tissues. While many genes and pathways necessary for regulating angiogenesis have been identified, those responsible for endothelial cell (EC) survival during angiogenesis remain largely unknown. We have investigated the in vivo role of myeloid cell leukemia 1 (MCL1), a pro-survival member of the BCL2 family, in EC survival during angiogenesis. EC-specific deletion of Mcl1 resulted in a dose-dependent increase in EC apoptosis in the angiogenic vasculature and a corresponding decline in vessel density. Our results suggest this apoptosis was independent of the BH3-only protein BIM. Despite the known link between apoptosis and blood vessel regression, this was not the cause of reduced vessel density observed in the absence of endothelial MCL1. Rather, the reduction in vessel density was linked to ectopic apoptosis in regions of the angiogenic vasculature where EC proliferation and new vessel growth occurs. We have therefore identified MCL1 as an essential survival factor for ECs that is required for blood vessel production during angiogenesis.

Indexed as

AnimalsApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinBcl-2-Like Protein 11Caspase 3Cells, CulturedCell SurvivalCollagen Type IVEmbryo, MammalianEndothelial CellsKidneyMiceMice, Inbred C57BLMice, KnockoutMyeloid Cell Leukemia Sequence 1 Proteinbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinBcl-2-Like Protein 11Caspase 3Collagen Type IVMyeloid Cell Leukemia Sequence 1 ProteinPlatelet Endothelial Cell Adhesion Molecule-1

Identifiers

PMID26943318
PMCPMC4947668
OpenAlexW2312423438

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.