Evidence map›Paper›PMID 29101235›Full record

ArticleThe Journal of biological chemistry2017

Mechanisms and modulation of microvesicle uptake in a model of alveolar cell communication.

Daniel J Schneider, Jennifer M Speth, Loka R Penke, Scott H Wettlaufer, Joel A Swanson, Marc Peters-Golden

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 78 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

6 authors at 2 institutions in 1 country.

Daniel J SchneiderFrom the Division of Pulmonary and Critical Care Medicine.
Jennifer M SpethFrom the Division of Pulmonary and Critical Care Medicine.
Loka R PenkeFrom the Division of Pulmonary and Critical Care Medicine.
Scott H WettlauferFrom the Division of Pulmonary and Critical Care Medicine.
Joel A SwansonDepartment of Microbiology and Immunology, and.
Marc Peters-GoldenFrom the Division of Pulmonary and Critical Care Medicine, petersm@umich.edu.
Pulmonary and Critical Care Associates · USUniversity of Michigan–Ann Arbor · US

Funding

Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
Control of Fibroblast Function by Prostaglandin E2 and Plasminogen ActivationR01HL094311 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2009 to 2017
$3.4M
Secreted SOCS Proteins as Vectors of Lung Macrophage to Epithelial Cell CrosstalkR01HL125555 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2015 to 2018
$2.2M
The Regulation of MacropinocytosisR01GM110215 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SWANSON, JOEL A · 2014 to 2017
$1.3M
Inducible Renitence in MacrophagesR01GM101189 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SWANSON, JOEL A · 2013 to 2016
$1.2M
NCATS NIH HHS UL1 TR000433NHLBI NIH HHS R01 HL094311NHLBI NIH HHS R01 HL125555NHLBI NIH HHS T32 HL007749NIGMS NIH HHS R01 GM101189NIGMS NIH HHS R01 GM110215
6 · The paper itself

Abstract

Extracellular vesicles, including exosomes and shed microvesicles (MVs), can be internalized by recipient cells to modulate function. Although the mechanism by which extracellular vesicles are internalized is incompletely characterized, it is generally considered to involve endocytosis and an initial surface-binding event. Furthermore, modulation of uptake by microenvironmental factors is largely unstudied. Here, we used flow cytometry, confocal microscopy, and pharmacologic and molecular targeting to address these gaps in knowledge in a model of pulmonary alveolar cell-cell communication. Alveolar macrophage-derived MVs were fully internalized by alveolar epithelial cells in a time-, dose-, and temperature-dependent manner. Uptake was dependent on dynamin and actin polymerization. However, it was neither saturable nor dependent on clathrin or receptor binding. Internalization was enhanced by extracellular proteins but was inhibited by cigarette smoke extract via oxidative disruption of actin polymerization. We conclude that MV internalization occurs via a pathway more consistent with fluid-phase than receptor-dependent endocytosis and is subject to bidirectional modulation by relevant pathologic perturbations.

Indexed as

ActinsAcute Lung InjuryAlveolar Epithelial CellsAnimalsCell CommunicationCell-Derived MicroparticlesCell LineDynaminsEndocytosisFemaleLigandsMacrophages, AlveolarModels, BiologicalNicotianaOxidation-ReductionRatsActinsDynaminsLigandsReceptors, Cell SurfaceSmokeactinalbuminalveolarendocytosisepithelialextracellular vesiclesmacrophagemacropinocytosisoxidation

Identifiers

PMID29101235
PMCPMC5743066
OpenAlexW2766731631

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.