Evidence map›Paper›PMID 26980205›Full record

ArticleCardiovascular research2016

Exosomes induce and reverse monocrotaline-induced pulmonary hypertension in mice.

Jason M Aliotta, Mandy Pereira, Sicheng Wen, Mark S Dooner, Michael Del Tatto, Elaine Papa, Laura R Goldberg, Grayson L Baird, Corey E Ventetuolo, Peter J Quesenberry and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 1 pooled it
14.6field-weighted citation impact, top 1% 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

154 citing papers in PubMed, 1 synthesis or guideline pooled it, 252 citations in OpenAlex.

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94 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Jason M AliottaDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI 02903, USA jason_aliotta@brown.edu jaliotta@lifespan.org.
Mandy PereiraDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
Sicheng WenDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
Mark S DoonerDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
Michael Del TattoDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
Elaine PapaDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
Laura R GoldbergDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
Grayson L BairdLifespan Biostatistics Core, Rhode Island Hospital, Providence, RI 02903, USA.
Corey E VentetuoloDepartment of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI 02903, USA.
Peter J QuesenberryDepartment of Medicine, Division of Hematology/Oncology, Rhode Island Hospital, Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA.
James R KlingerDepartment of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI 02903, USA.
Rhode Island Hospital · USBrown University · USProvidence College · US

Funding

Uncoupling of IL-1 beta and VEGF-A Crosstalk Contributes to Impaired Arteriogenesis Response to Ischemia in Chronic Diabetes MellitusP20GM103652 · NIGMS · OCEAN STATE RESEARCH INSTITUTE, INC. · PI ROUNDS, SHARON IRENE SMITH · 2013 to 2022
$21.3M
TYORISINE PHOSPHATASE SHP2 IN HEMATOPOIETIC STEM CELL PROPERTY MAINTENANCEP20RR025179 · NCRR · RHODE ISLAND HOSPITAL · PI RAMRATNAM, BHARAT · 2009 to 2011
$6.4M
Stem Cell Biology: New Directions in Clinical and Basic ResearchP20GM103468 · NIGMS · RHODE ISLAND HOSPITAL · PI QUESENBERRY, PETER J. · 2012 to 2013
$4.5M
Natriuretic Peptides in Pulmonary Endothelial Cell Barrier FunctionR01HL088328 · NHLBI · RHODE ISLAND HOSPITAL · PI KLINGER, JAMES RAYMOND · 2007 to 2011
$1.6M
NCRR NIH HHS P20 RR025179NHLBI NIH HHS R01 HL088328NIGMS NIH HHS P20 GM103468NIGMS NIH HHS P20 GM103652
6 · The paper itself

Abstract

aimsExtracellular vesicles (EVs) from mice with monocrotaline (MCT)-induced pulmonary hypertension (PH) induce PH in healthy mice, and the exosomes (EXO) fraction of EVs from mesenchymal stem cells (MSCs) can blunt the development of hypoxic PH. We sought to determine whether the EXO fraction of EVs is responsible for modulating pulmonary vascular responses and whether differences in EXO-miR content explains the differential effects of EXOs from MSCs and mice with MCT-PH. METHODS AND

resultsPlasma, lung EVs from MCT-PH, and control mice were divided into EXO (exosome), microvesicle (MV) fractions and injected into healthy mice. EVs from MSCs were divided into EXO, MV fractions and injected into MCT-treated mice. PH was assessed by right ventricle-to-left ventricle + septum (RV/LV + S) ratio and pulmonary arterial wall thickness-to-diameter (WT/D) ratio. miR microarray analyses were also performed on all EXO populations. EXOs but not MVs from MCT-injured mice increased RV/LV + S, WT/D ratios in healthy mice. MSC-EXOs prevented any increase in RV/LV + S, WT/D ratios when given at the time of MCT injection and reversed the increase in these ratios when given after MCT administration. EXOs from MCT-injured mice and patients with idiopathic pulmonary arterial hypertension (IPAH) contained increased levels of miRs-19b,-20a,-20b, and -145, whereas miRs isolated from MSC-EXOs had increased levels of anti-inflammatory, anti-proliferative miRs including miRs-34a,-122,-124, and -127.

conclusionThese findings suggest that circulating or MSC-EXOs may modulate pulmonary hypertensive effects based on their miR cargo. The ability of MSC-EXOs to reverse MCT-PH offers a promising potential target for new PAH therapies.

Indexed as

Mesenchymal Stem Cell TransplantationMonocrotalineVascular RemodelingAnimalsCase-Control StudiesCell-Derived MicroparticlesCells, CulturedDisease Models, AnimalExosomesFamilial Primary Pulmonary HypertensionGene Expression RegulationHumansHypertension, PulmonaryHypertrophy, Right VentricularMaleMesenchymal Stem CellsMicroRNAsMonocrotalineExosomesExtracellular vesiclesMesenchymal stem cellsMicroRNAPulmonary hypertension

Identifiers

PMID26980205
PMCPMC4872877
OpenAlexW2296979020

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.