Evidence map›Paper›PMID 25387407›Full record

ArticleStem cells and development2015

Signaling via PI3K/FOXO1A pathway modulates formation and survival of human embryonic stem cell-derived endothelial cells.

Béla Merkely, Edit Gara, Zsuzsanna Lendvai, Judit Skopál, Thomas Leja, Wenhua Zhou, Annamária Kosztin, György Várady, Maxime Mioulane, Zsolt Bagyura and 3 more

Open access · greenAbstract read
In one paragraph

Article in Stem cells and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Annatto (Biomolecules · 2019
    Article
  5. FOXOs in cancer immunity: Knowns and unknowns.Seminars in cancer biology · 2018
    Review
  6. Review
  7. Article
  8. FoxO proteins in the nervous system.Analytical cellular pathology (Amsterdam) · 2015
    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

13 authors at 3 institutions in 3 countries.

Béla Merkely1 Heart and Vascular Center, Semmelweis University , Budapest, Hungary .
Edit Gara
Zsuzsanna Lendvai
Judit Skopál
Thomas Leja
Wenhua Zhou
Annamária Kosztin
György Várady
Maxime Mioulane
Zsolt Bagyura
Tamás Németh
Sian E Harding
Gábor Földes
Semmelweis University · HULung Institute · USMembrane Technology & Research (United States) · US

Funding

British Heart Foundation RG/14/1/30588Medical Research Council MR/L012618/1National Centre for the Replacement, Refinement and Reduction of Animals in Research G1000035/1
6 · The paper itself

Abstract

Vascular derivatives of human embryonic stem cells (hESC) are being developed as sources of tissue-specific cells for organ regeneration. However, identity of developmental pathways that modulate the specification of endothelial cells is not known yet. We studied phosphatidylinositol 3-kinase (PI3K)-Forkhead box O transcription factor 1A (FOXO1A) pathways during differentiation of hESC toward endothelial lineage and on proliferation, maturation, and cell death of hESC-derived endothelial cells (hESC-EC). During differentiation of hESC, expression of FOXO1A transcription factor was linked to the expression of a cluster of angiogenesis- and vascular remodeling-related genes. PI3K inhibitor LY294002 activated FOXO1A and induced formation of CD31(+) hESC-EC. In contrast, differentiating hESC with silenced FOXO1A by small interfering RNA (siRNA) showed lower mRNA levels of CD31 and angiopoietin2. LY294002 decreased proliferative activity of purified hESC-EC, while FOXO1A siRNA increased their proliferation. LY294002 inhibits migration and tube formation of hESC-EC; in contrast, FOXO1A siRNA increased in vitro tube formation activity of hESC-EC. After in vivo conditioning of cells in athymic nude rats, cells retain their low FOXO1A expression levels. PI3K/FOXO1A pathway is important for function and survival of hESC-EC and in the regulation of endothelial cell fate. Understanding these properties of hESC-EC may help in future applications for treatment of injured organs.

Indexed as

Cell DifferentiationSignal TransductionAnimalsCells, CulturedEmbryonic Stem CellsForkhead Box Protein O1Forkhead Transcription FactorsHumansHuman Umbilical Vein Endothelial CellsNeovascularization, PhysiologicPhosphatidylinositol 3-KinasesRatsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanPhosphatidylinositol 3-Kinases

Identifiers

PMID25387407
PMCPMC4367527
OpenAlexW2317020025

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.