Evidence map›Paper›PMID 30442193›Full record

ArticleStem cell research & therapy2018

The prostaglandin H2 analog U-46619 improves the differentiation efficiency of human induced pluripotent stem cells into endothelial cells by activating both p38MAPK and ERK1/2 signaling pathways.

Liping Su, Xiaocen Kong, Szeyun Lim, Szejie Loo, Shihua Tan, Kiankeong Poh, James Dutton, Colin Stewart, Stuart Cook, Xiaofei Su and 3 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  12. Cardiac Tissue Engineering for the Treatment of Myocardial Infarction.Journal of cardiovascular development and disease · 2021
    Review
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  18. Qingxin Kaiqiao Fang Inhibits AEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  19. 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

13 authors at 6 institutions in 4 countries.

Liping SuNational Heart Research Institute of Singapore, National Heart Centre Singapore, Singapore, 117609, Singapore.
Xiaocen KongDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, 210006, China.
Szeyun LimNational Heart Research Institute of Singapore, National Heart Centre Singapore, Singapore, 117609, Singapore.
Szejie LooNational Heart Research Institute of Singapore, National Heart Centre Singapore, Singapore, 117609, Singapore.
Shihua TanNational Heart Research Institute of Singapore, National Heart Centre Singapore, Singapore, 117609, Singapore.
Kiankeong PohDepartment of Cardiology, National University Health System Singapore and Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
James DuttonStem cell Institute, University of Minnesota, Minneapolis, MN, USA.
Colin StewartInstitute of Medical Biology, A*STAR, Singapore, Singapore.
Stuart CookNational Heart Research Institute of Singapore, National Heart Centre Singapore, Singapore, 117609, Singapore.
Xiaofei SuDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, 210006, China.
Jianhua MaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, 210006, China. majianhua@china.com.
Jianyi ZhangDepartment of Biomedical Engineering, The University of Alabama at Birmingham, Birmingham, AL, 35294-2182, USA. jayzhang@uab.edu.
Lei YeNational Heart Research Institute of Singapore, National Heart Centre Singapore, Singapore, 117609, Singapore. yeleislp@yahoo.com.ORCID 0000-0001-5039-6224
National Heart Centre Singapore · SGNanjing Medical University · CNNational University of Singapore · SGAgency for Science, Technology and Research · SGUniversity of Alabama at Birmingham · USUniversity of Minnesota · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
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
Supplement of HL131017: Myocardial remuscularization by cardiac patch delivery of epicardial FSTL1 and CCND2 overexpressing cardiomyocytesR01HL131017 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SERPOOSHAN, VAHID, ZHANG, JIANYI · 2016 to 2025
$5.8M
Endogenous and exogenous mechanisms that promote myocardial remuscularization in post infarction LV remodelingR01HL114120 · NHLBI · UNIVERSITY OF MINNESOTA · PI ZHANG, JIANYI · 2012 to 2021
$5.6M
NHLBI NIH HHS R01 HL114120NHLBI NIH HHS R01 HL131017NHLBI NIH HHS U01 HL134764NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

backgroundWe have shown that the differentiation of human-induced pluripotent stem cells (hiPSCs) into endothelial cells (ECs) is more efficient when performed with a 3-dimensional (3D) scaffold of biomaterial than in monolayers. The current study aims to further increase hiPSC-EC differentiation efficiency by deciphering the signaling pathways in 3D scaffolds. METHODS AND

resultsWe modified our 3D protocol by using U-46619 to upregulate both p38 mitogen-activated protein kinase (p38MAPK) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling, which increased the differentiation efficiency (as measured by CD31 expression) to as high as 89% in two established hiPSC lines. The differentiated cells expressed arteriovenous, but not lymphatic, markers; formed tubular structures and EC lumen in vitro; had significantly shorter population-doubling times than monolayer-differentiated hiPSC-ECs; and restored perfusion and vascularity in a murine hind limb ischemia model. The differentiation efficiency was also > 85% in three hiPSC lines that had been derived from patients with diseases or disease symptoms that have been linked to endothelial dysfunction.

conclusionsThese observations demonstrate that activating both p38MAPK and ERK1/2 signaling pathways with U-46619 improves the efficiency of arteriovenous hiPSC-EC differentiation and produces cells with greater proliferative capacity.

Indexed as

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidAnimalsCell DifferentiationCell LineDisease Models, AnimalEndothelial CellsEnzyme ActivationHindlimbHumansInduced Pluripotent Stem CellsIschemiaMAP Kinase Signaling SystemMesodermMice, Inbred NODMice, SCIDp38 Mitogen-Activated Protein Kinases15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidChir 99021p38 Mitogen-Activated Protein KinasesPyridinesPyrimidinesEndothelial differentiationHuman-induced pluripotent stem cellsSignaling pathways

Identifiers

PMID30442193
PMCPMC6238266
OpenAlexW2901152489

What OpenQuestion holds

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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.