Evidence map›Paper›PMID 27642005›Full record

ArticleScientific reports2016

Nox2 contributes to the arterial endothelial specification of mouse induced pluripotent stem cells by upregulating Notch signaling.

Xueling Kang, Xiangxiang Wei, Xinhong Wang, Li Jiang, Cong Niu, Jianyi Zhang, Sifeng Chen, Dan Meng

Abstract read
In one paragraph

Article in Scientific reports, 2016. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Hydrogen Peroxide and Redox Regulation of Developments.Antioxidants (Basel, Switzerland) · 2018
    Review
  10. NOTCH regulation of the endothelial cell phenotype.Current opinion in hematology · 2018
    Review
  11. Review
  12. Essentiality of Regulator of G Protein Signaling 6 and Oxidized CaJournal of the American Heart Association · 2017
    Article
  13. NADPH Oxidases, Angiogenesis, and Peripheral Artery Disease.Antioxidants (Basel, Switzerland) · 2017
    Review
  14. 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

8 authors.

Xueling KangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Xiangxiang WeiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Xinhong WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Li JiangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Cong NiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Jianyi ZhangDivision of Cardiology, Department of Medicine, Stem Cell Institute, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
Sifeng ChenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Dan MengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.

Funding

Integrated Cellular and Tissue Engineering for Ischemic Heart DiseaseU01HL134764 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BURSAC, NENAD, KAMP, TIMOTHY J. · 2016 to 2022
$7.7M
NHLBI NIH HHS U01 HL134764
6 · The paper itself

Abstract

Reactive oxygen species (ROS) have a crucial role in stem-cell differentiation; however, the mechanisms by which ROS regulate the differentiation of stem cells into endothelial cells (ECs) are unknown. Here, we determine the role of ROS produced by NADPH oxidase 2 (Nox2) in the endothelial-lineage specification of mouse induced-pluripotent stem cells (miPSCs). When wild-type (WT) and Nox2-knockout (Nox2(-/-)) miPSCs were differentiated into ECs (miPSC-ECs), the expression of endothelial markers, arterial endothelial markers, pro-angiogenic cytokines, and Notch pathway components was suppressed in the Nox2(-/-) cells but increased in both WT and Nox2(-/-) miPSCs when Nox2 expression was upregulated. Higher levels of Nox2 expression increased Notch signaling and arterial EC differentiation, and this increase was abolished by the inhibition of ROS generation or by the silencing of Notch1 expression. Nox2 deficiency was associated with declines in the survival and angiogenic potency of miPSC-ECs, and capillary and arterial density were lower in the ischemic limbs of mice after treatment with Nox2(-/-) miPSC-ECs than WT miPSC-EC treatment. Taken together, these observations indicate that Nox2-mediated ROS production promotes arterial EC specification in differentiating miPSCs by activating the Notch signaling pathway and contributes to the angiogenic potency of transplanted miPSC-derived ECs.

Indexed as

Cell DifferentiationSignal TransductionAnimalsArteriesEndothelial CellsInduced Pluripotent Stem CellsMiceMice, KnockoutNADPH Oxidase 2Reactive Oxygen SpeciesReceptors, NotchCybb protein, mouseNADPH Oxidase 2Reactive Oxygen SpeciesReceptors, Notch

Identifiers

PMID27642005
PMCPMC5027389

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Registered trials

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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.