Evidence map›Paper›PMID 28486752›Full record

ArticlePediatric pulmonology2017

Exosomes contribute to endothelial integrity and acute chest syndrome risk: Preliminary findings.

Gabrielle Lapping-Carr, Abdelnaby Khalyfa, Stephanie Rangel, Wendy Darlington, Eric C Beyer, Radhika Peddinti, John M Cunningham, David Gozal

Abstract read
In one paragraph

Article in Pediatric pulmonology, 2017. 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
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Extracellular Vesicles in Sickle Cell Disease: A Promising Tool.Bioengineering (Basel, Switzerland) · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Endothelial Barrier Integrity Is DisruptedFrontiers in immunology · 2020
    Article
  11. Article
  12. Review
  13. Article
  14. Measuring success: utility of biomarkers in sickle cell disease clinical trials and care.Hematology. American Society of Hematology. Education Program · 2018
    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 at 2 institutions in 1 country.

Gabrielle Lapping-CarrSections of Pediatric Hematology-Oncology,, Department of Pediatrics, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.ORCID http://orcid.org/0000-0002-6185-1605
Abdelnaby KhalyfaDepartment of Pediatrics, Section of Pediatric, Pulmonology and Sleep Medicine, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
Stephanie RangelDepartment of Dermatology, Northwestern University, Chicago, Illinois.
Wendy DarlingtonSections of Pediatric Hematology-Oncology,, Department of Pediatrics, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
Eric C BeyerSections of Pediatric Hematology-Oncology,, Department of Pediatrics, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
Radhika PeddintiSections of Pediatric Hematology-Oncology,, Department of Pediatrics, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
John M CunninghamSections of Pediatric Hematology-Oncology,, Department of Pediatrics, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
David GozalDepartment of Pediatrics, Section of Pediatric, Pulmonology and Sleep Medicine, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
Comer Children's Hospital · USNorthwestern University · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Training of Junior Faculty for Careers in Omics of Lung DiseasesK12HL119995 · NHLBI · UNIVERSITY OF CHICAGO · PI GOZAL, DAVID, GROSSMAN, ROBERT L. · 2013 to 2017
$1.3M
NCATS NIH HHS UL1 TR000430NHLBI NIH HHS K12 HL119995
6 · The paper itself

Abstract

backgroundAcute Chest Syndrome (ACS) is one of the leading causes of death among children with Sickle Cell Disease (SCD). Disruption of microvascular integrity is critical to the pathophysiology of ACS, but the factors governing its phenotypic variability are incompletely understood. Because circulating exosomes have been implicated in vascular dysfunction in various diseases, we hypothesized that exosomes induce endothelial dysfunction in patients who experience ACS. PROCEDURE: Cross-sectional cohort study including 33 outpatients with SCD (without new health-related complaints or recent transfusions) and a cohort of control patients. Exosomes were isolated from platelet-free plasma.

resultsImageStream showed that exosome counts were greatly increased in patients with SCD compared with controls, but there were few differences in the concentrations of exosomes between patients who had experienced ACS (ACS(+)) and those who had not (ACS(-)). Exosomes were added to human microvascular endothelial cells, and the exosomal effects on monolayer integrity was determined using Electric Cell-substrate Impedance Sensing (ECIS). Exosomes from SCD patients without ACS differed minimally from control patients; however, exosomes from ACS(+) decreased endothelial cell resistance compared to ACS(-), (Relative resistance: ACS(+): 0.981 ± 0.055 vs ACS(-): 1.124 ± 0.042; P = 0.006). Treatment of endothelial cultures with exosomes from ACS(-) patients increased endothelial Nitric Oxide Synthase (eNOS) mRNA expression, while ACS(+)-derived exosomes were not able to increase eNOS expression above that of controls.

conclusionsThese findings demonstrate that patients with SCD have circulating exosomes that produce differential effects that may contribute to the pathophysiology of ACS and may serve as risk-related biomarkers.

Indexed as

ExosomesAcute Chest SyndromeAdolescentAdultAnemia, Sickle CellCells, CulturedChildChild, PreschoolCohort StudiesCross-Sectional StudiesEndothelial CellsFemaleHumansMaleNitric Oxide Synthase Type IIIRiskNitric Oxide Synthase Type IIINOS3 protein, humanRNA, Messengerbiomarkerslung pathologysickle cell disease

Identifiers

PMID28486752
PMCPMC5653417
OpenAlexW2612321063

What OpenQuestion holds

Textmetadata
LicenceTDM
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.