Evidence map›Paper›PMID 23963623›Full record

ArticleStem cells (Dayton, Ohio)2014

Akt suppression of TGFβ signaling contributes to the maintenance of vascular identity in embryonic stem cell-derived endothelial cells.

Edo Israely, Michael Ginsberg, Daniel Nolan, Bi-Sen Ding, Daylon James, Olivier Elemento, Shahin Rafii, Sina Y Rabbany

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. cAMP/EPAC Signaling Enables ETV2 to Induce Endothelial Cells with High Angiogenesis Potential.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  2. Article
  3. Article
  4. TGF-β Signaling in Control of Cardiovascular Function.Cold Spring Harbor perspectives in biology · 2018
    Review
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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

8 authors at 4 institutions in 1 country.

Edo IsraelyDepartment of Genetic Medicine, Ansary Stem Cell Institute, Howard Hughes Medical Institute, Weill Cornell Medical College, New York, New York, USA.
Michael Ginsberg
Daniel Nolan
Bi-Sen Ding
Daylon James
Olivier Elemento
Shahin Rafii
Sina Y Rabbany
Cornell University · USAngiocrine Bioscience (United States) · USHoward Hughes Medical Institute · USHofstra University · US

Funding

VASCULAR BIOCHEMISTRY AND ATHEROSCLEROSIST32HL007423 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI HAJJAR, KATHERINE AMBERSON · 1985 to 2009
$2.4M
Identification of vascular inductive signals in liver regenerationR01DK095039 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI RAFII, SHAHIN · 2012 to 2016
$2.2M
Contribution of the vascular niche to the hematopoietic reconstitution.R01HL097797 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI RAFII, SHAHIN · 2009 to 2012
$1.7M
Howard Hughes Medical InstituteNHLBI NIH HHS HL007423NHLBI NIH HHS R01 HL097797NHLBI NIH HHS R01S HL097797NHLBI NIH HHS T32 HL007423NIDDK NIH HHS DK095039NIDDK NIH HHS R01 DK095039
6 · The paper itself

Abstract

The ability to generate and maintain stable in vitro cultures of mouse endothelial cells (ECs) has great potential for genetic dissection of the numerous pathologies involving vascular dysfunction as well as therapeutic applications. However, previous efforts at achieving sustained cultures of primary stable murine vascular cells have fallen short, and the cellular requirements for EC maintenance in vitro remain undefined. In this study, we have generated vascular ECs from mouse embryonic stem (ES) cells and show that active Akt is essential to their survival and propagation as homogeneous monolayers in vitro. These cells harbor the phenotypical, biochemical, and functional characteristics of ECs and expand throughout long-term cultures, while maintaining their angiogenic capacity. Moreover, Akt-transduced embryonic ECs form functional perfused vessels in vivo that anastomose with host blood vessels. We provide evidence for a novel function of Akt in stabilizing EC identity, whereby the activated form of the protein protects mouse ES cell-derived ECs from TGFβ-mediated transdifferentiation by downregulating SMAD3. These findings identify a role for Akt in regulating the developmental potential of ES cell-derived ECs and demonstrate that active Akt maintains endothelial identity in embryonic ECs by interfering with active TGFβ-mediated processes that would ordinarily usher these cells to alternate fates.

Indexed as

AnimalsCell DifferentiationCells, CulturedEmbryonic Stem CellsEndothelial CellsMiceProto-Oncogene Proteins c-aktSignal TransductionTransforming Growth Factor betaProto-Oncogene Proteins c-aktTransforming Growth Factor betaAktEmbryonicEndothelialSMAD3Stem

Identifiers

PMID23963623
PMCPMC4886558
OpenAlexW1905855640

What OpenQuestion holds

Textmetadata
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.