Evidence map›Paper›PMID 28191769›Full record

ArticleStem cells translational medicine2017

Suppression of Transforming Growth Factor-β Signaling Delays Cellular Senescence and Preserves the Function of Endothelial Cells Derived from Human Pluripotent Stem Cells.

Hao Bai, Yongxing Gao, Dixie L Hoyle, Tao Cheng, Zack Z Wang

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  13. Vascular progenitor cell senescence in patients with Marfan syndrome.Journal of cellular and molecular medicine · 2019
    Article
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  17. Review
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  19. Article
  20. Techniques to Induce and Quantify Cellular Senescence.Journal of visualized experiments : JoVE · 2017
    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.

Hao BaiDivision of Hematology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yongxing GaoDivision of Hematology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Dixie L HoyleDivision of Hematology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tao ChengState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Disease Hospital, Chinese Academy of Medical Sciences, Tianjin, People's Republic of China.
Zack Z WangDivision of Hematology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USTianjin University of Technology · CNJohns Hopkins Medicine · US

Funding

Generation of engraftable HSPCs from hemogenic endothelial cellsR01DK106109 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WANG, ZACK Z. · 2016 to 2018
$875k
NIDDK NIH HHS R01 DK106109
6 · The paper itself

Abstract

Transplantation of vascular cells derived from human pluripotent stem cells (hPSCs) offers an attractive noninvasive method for repairing the ischemic tissues and for preventing the progression of vascular diseases. Here, we found that in a serum-free condition, the proliferation rate of hPSC-derived endothelial cells is quickly decreased, accompanied with an increased cellular senescence, resulting in impaired gene expression of endothelial nitric oxide synthase (eNOS) and impaired vessel forming capability in vitro and in vivo. To overcome the limited expansion of hPSC-derived endothelial cells, we screened small molecules for specific signaling pathways and found that inhibition of transforming growth factor-β (TGF-β) signaling significantly retarded cellular senescence and increased a proliferative index of hPSC-derived endothelial cells. Inhibition of TGF-β signaling extended the life span of hPSC-derived endothelial and improved endothelial functions, including vascular network formation on Matrigel, acetylated low-density lipoprotein uptake, and eNOS expression. Exogenous transforming growth factor-β1 increased the gene expression of cyclin-dependent kinase inhibitors, p15

Indexed as

AnimalsBenzamidesCell LineCell ProliferationCellular SenescenceCulture Media, Serum-FreeCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DioxolesDisease Models, AnimalEndothelial Progenitor CellsHuman Embryonic Stem CellsHumansIschemiaLipoproteins, LDL4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideacetyl-LDLBenzamidesCDKN1A protein, humanCDKN2A protein, humanCDKN2B protein, humanCulture Media, Serum-FreeCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DioxolesLipoproteins, LDLNitric Oxide Synthase Type IIINOS3 protein, humanReceptor, Transforming Growth Factor-beta Type ITGFB1 protein, humanTGFBR1 protein, humanTransforming Growth Factor betaTransforming Growth Factor beta1Endothelial cellsHuman pluripotent stem cellsSenescenceTransforming growth factor-β

Identifiers

PMID28191769
PMCPMC5442820
OpenAlexW2522449792

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.