Evidence map›Paper›PMID 26743080›Full record

ArticleJournal of cell science2016

Loss of PPARγ in endothelial cells leads to impaired angiogenesis.

Sanna Vattulainen-Collanus, Oyediran Akinrinade, Molong Li, Minna Koskenvuo, Caiyun Grace Li, Shailaja P Rao, Vinicio de Jesus Perez, Ke Yuan, Hirofumi Sawada, Juha W Koskenvuo and 3 more

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

Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

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  15. Deciphering Intratumoral Molecular Heterogeneity in Clear Cell Renal Cell Carcinoma with a Radiogenomics Platform.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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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

13 authors at 5 institutions in 3 countries.

Sanna Vattulainen-CollanusChildren's Hospital Helsinki, Pediatric Cardiology, University of Helsinki and Helsinki University Central Hospital, Helsinki 00290, Finland.
Oyediran AkinrinadeChildren's Hospital Helsinki, Pediatric Cardiology, University of Helsinki and Helsinki University Central Hospital, Helsinki 00290, Finland Institute of Biomedicine, University of Helsinki, Helsinki 00290, Finland.
Molong LiThe Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA Research Center of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku 20520, Finland.
Minna KoskenvuoChildren's Hospital Helsinki, Division of Hematology-Oncology and Stem Cell Transplantation, University of Helsinki and Helsinki University Central Hospital, 00290 Helsinki, Finland.
Caiyun Grace LiDepartment of Pediatrics, Wall Center for Pulmonary Vascular Disease, Cardiovascular Institute Stanford University, Stanford, CA 94305, USA.
Shailaja P RaoDepartment of Pediatrics, Wall Center for Pulmonary Vascular Disease, Cardiovascular Institute Stanford University, Stanford, CA 94305, USA.
Vinicio de Jesus PerezDivision of Pulmonary and Critical Care Medicine, Stanford University, Stanford, CA 94305, USA.
Ke YuanDivision of Pulmonary and Critical Care Medicine, Stanford University, Stanford, CA 94305, USA.
Hirofumi SawadaDepartment of Pediatrics, Wall Center for Pulmonary Vascular Disease, Cardiovascular Institute Stanford University, Stanford, CA 94305, USA Department of Pediatrics, Mie University Graduate School of Medicine, Mie 5148507, Japan.
Juha W KoskenvuoResearch Center of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku 20520, Finland Department of Clinical Physiology and Nuclear Medicine, HUS Medical Imaging Center, Helsinki University Central Hospital and University of Helsinki, 00290 Helsinki, Finland.
Cristina AlviraDepartment of Pediatrics, Wall Center for Pulmonary Vascular Disease, Cardiovascular Institute Stanford University, Stanford, CA 94305, USA.
Marlene RabinovitchDepartment of Pediatrics, Wall Center for Pulmonary Vascular Disease, Cardiovascular Institute Stanford University, Stanford, CA 94305, USA.
Tero-Pekka AlastaloChildren's Hospital Helsinki, Pediatric Cardiology, University of Helsinki and Helsinki University Central Hospital, Helsinki 00290, Finland tero-pekka.alastalo@helsinki.fi.
University of Helsinki · FIStanford University · USCardiovascular Institute of the South · USJohns Hopkins University · USMie University · JP

Funding

Pulmonary Hypertension in Genetically Modified MiceR01HL074186 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2004 to 2022
$10.4M
The BMP-PPARy Axis and Pulmonary HypertensionR01HL087118 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2008 to 2022
$7.2M
Novel Molecular Mechanisms Regulating Postnatal Pulmonary AngiogenesisR01HL122918 · NHLBI · STANFORD UNIVERSITY · PI ALVIRA, CRISTINA MARIA · 2014 to 2018
$2.3M
NHLBI NIH HHS R01 HL074186NHLBI NIH HHS R01-HL074186NHLBI NIH HHS R01 HL087118NHLBI NIH HHS R01-HL087118NHLBI NIH HHS R01 HL122918
6 · The paper itself

Abstract

Tie2-promoter-mediated loss of peroxisome proliferator-activated receptor gamma (PPARγ, also known as PPARG) in mice leads to osteopetrosis and pulmonary arterial hypertension. Vascular disease is associated with loss of PPARγ in pulmonary microvascular endothelial cells (PMVEC); we evaluated the role of PPARγ in PMVEC functions, such as angiogenesis and migration. The role of PPARγ in angiogenesis was evaluated in Tie2CrePPARγ(flox/flox) and wild-type mice, and in mouse and human PMVECs. RNA sequencing and bioinformatic approaches were utilized to reveal angiogenesis-associated targets for PPARγ. Tie2CrePPARγ(flox/flox) mice showed an impaired angiogenic capacity. Analysis of endothelial progenitor-like cells using bone marrow transplantation combined with evaluation of isolated PMVECs revealed that loss of PPARγ attenuates the migration and angiogenic capacity of mature PMVECs. PPARγ-deficient human PMVECs showed a similar migration defect in culture. Bioinformatic and experimental analyses newly revealed E2F1 as a target of PPARγ in the regulation of PMVEC migration. Disruption of the PPARγ-E2F1 axis was associated with a dysregulated Wnt pathway related to the GSK3B interacting protein (GSKIP). In conclusion, PPARγ plays an important role in sustaining angiogenic potential in mature PMVECs through E2F1-mediated gene regulation.

Indexed as

Animalsbeta CateninBone Marrow TransplantationCell MovementCells, CulturedE2F1 Transcription FactorEndothelial CellsEndothelium, VascularGene ExpressionHumansLungMiceMice, TransgenicNeovascularization, PhysiologicPPAR gammaTranscriptional Activationbeta CateninCTNNB1 protein, mouseE2f1 protein, mouseE2F1 Transcription FactorPPAR gammaAngiogenesisE2F1Endothelial cellGSKIPOsteopetrosisPPARγPulmonary hypertensionWnt signaling

Identifiers

PMID26743080
PMCPMC5108588
OpenAlexW2260545875

What OpenQuestion holds

Textmetadata
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.