Evidence map›Paper›PMID 27866874›Full record

ArticleStem cell reports2016

PAR1 Scaffolds TGFβRII to Downregulate TGF-β Signaling and Activate ESC Differentiation to Endothelial Cells.

Haixia Gong, Shejuan An, Antonia Sassmann, Menglin Liu, Victoria Mastej, Manish Mittal, Wei Zhang, Zhigang Hong, Stefan Offermanns, Jalees Rehman and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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

11 authors at 5 institutions in 2 countries.

Haixia GongDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Shejuan AnDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Antonia SassmannDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.
Menglin LiuDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Victoria MastejDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Manish MittalDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Wei ZhangFeinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Zhigang HongDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Stefan OffermannsDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.
Jalees RehmanDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.
Asrar B MalikDepartment of Pharmacology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA; The Center for Lung and Vascular Biology, University of Illinois, College of Medicine, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA. Electronic address: abmalik@uic.edu.
University of Illinois Urbana-Champaign · USIllinois College · USMax Planck Institute for Heart and Lung Research · DEUniversity of Illinois Chicago · USNorthwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
TRPC6 Regulation of Lung Endothelial Barrier FunctionP01HL060678 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B. · 2000 to 2020
$40.1M
TRAINING PROGRAM IN LUNG BIOLOGY AND PATHOBIOLOGYT32HL007829 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DOLLY MEHTA · 1995 to 2026
$15.6M
THROMBIN-INDUCED PULMONARY VASCULAR PERMEABILITYR01HL045638 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KOMAROVA, YULIA A · 1991 to 2025
$12.0M
Mesenchymal-Endothelial Transition as a Homeostatic Regenerative Mechanism in Acute Lung InjuryR01HL090152 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B., REHMAN, JALEES · 2007 to 2019
$5.9M
Endothelial Regeneration Following Lung Vascular InjuryR01HL118068 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B., REHMAN, JALEES · 2014 to 2017
$2.4M
The role of mitochondria in embryonic stem cells.R01GM094220 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI REHMAN, JALEES · 2011 to 2015
$1.5M
NCI NIH HHS P30 CA060553NHLBI NIH HHS P01 HL060678NHLBI NIH HHS R01 HL045638NHLBI NIH HHS R01 HL090152NHLBI NIH HHS R01 HL118068NHLBI NIH HHS T32 HL007829NIGMS NIH HHS R01 GM094220
6 · The paper itself

Abstract

We studied the function of the G-protein-coupled receptor PAR1 in mediating the differentiation of mouse embryonic stem cells (mESCs) to endothelial cells (ECs) that are capable of inducing neovascularization. We observed that either deletion or activation of PAR1 suppressed mouse embryonic stem cell (mESC) differentiation to ECs and neovascularization in mice. This was mediated by induction of TGFβRII/TGFβRI interaction, forming an active complex, which in turn induced SMAD2 phosphorylation. Inhibition of TGF-β signaling in PAR1-deficient mESCs restored the EC differentiation potential of mESCs. Thus, PAR1 in its inactive unligated state functions as a scaffold for TGFβRII to downregulate TGF-β signaling, and thereby promote ESC transition to functional ECs. The PAR1 scaffold function in ESCs is an essential mechanism for dampening TGF-β signaling and regulating ESC differentiation.

Indexed as

Cell DifferentiationDown-RegulationAnimalsEndothelial CellsGene DeletionMiceMouse Embryonic Stem CellsProtein BindingProtein Serine-Threonine KinasesReceptor, PAR-1Receptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISignal TransductionTransforming Growth Factor betaProtein Serine-Threonine KinasesReceptor, PAR-1Receptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor betacell differentiationEmbryonic stem cellsEndothelial cellsGPCRG-protein-coupled receptorPAR1scaffolding proteinstem cellsTGF-β signaling

Identifiers

PMID27866874
PMCPMC5161529
OpenAlexW2551532429

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.