Evidence map›Paper›PMID 38907252›Full record

ArticleJournal of translational medicine2024

Regulation of vascular endothelial integrity by mesenchymal stem cell extracellular vesicles after hemorrhagic shock and trauma.

Mark Barry, Alpa Trivedi, Byron Miyazawa, Lindsay R Vivona, David Shimmin, Praneeti Pathipati, Callie Keane, Joseph Cuschieri, Shibani Pati

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Mark BarryDepartment of Surgery, University of California, San Francisco, 513 Parnassus Ave, San Francisco, CA, 94143, USA.ORCID 0000-0003-2353-3312
Alpa TrivediDepartment of Laboratory Medicine, University of California, San Francisco, 513 Parnassus Ave , San Francisco, CA, 94143, USA.
Byron MiyazawaDepartment of Laboratory Medicine, University of California, San Francisco, 513 Parnassus Ave , San Francisco, CA, 94143, USA.
Lindsay R VivonaDepartment of Laboratory Medicine, University of California, San Francisco, 513 Parnassus Ave , San Francisco, CA, 94143, USA.
David ShimminNanoCraft.US., 807 Aldo Ave, Suite-101, Santa Clara, CA, 95054, USA.
Praneeti PathipatiDepartment of Laboratory Medicine, University of California, San Francisco, 513 Parnassus Ave , San Francisco, CA, 94143, USA.
Callie KeaneDepartment of Laboratory Medicine, University of California, San Francisco, 513 Parnassus Ave , San Francisco, CA, 94143, USA.
Joseph CuschieriDepartment of Surgery, University of California, San Francisco, 513 Parnassus Ave, San Francisco, CA, 94143, USA.
Shibani PatiDepartment of Surgery, University of California, San Francisco, 513 Parnassus Ave, San Francisco, CA, 94143, USA. Shibani.Pati@ucsf.edu.

Funding

Modulation of Pulmonary Vascular Permeability and Inflammation by Mesenchymal Stem Cells (MSCs) in Hemorrhagic ShockR01GM111899 · NIGMS · VITALANT · PI PATI, SHIBANI · 2015 to 2019
$1.6M
Foundation for the National Institutes of Health R01GM111899NIGMS NIH HHS R01 GM111899
6 · The paper itself

Abstract

backgroundPatients with hemorrhagic shock and trauma (HS/T) are vulnerable to the endotheliopathy of trauma (EOT), characterized by vascular barrier dysfunction, inflammation, and coagulopathy. Cellular therapies such as mesenchymal stem cells (MSCs) and MSC extracellular vesicles (EVs) have been proposed as potential therapies targeting the EOT. In this study we investigated the effects of MSCs and MSC EVs on endothelial and epithelial barrier integrity in vitro and in vivo in a mouse model of HS/T. This study addresses the systemic effects of HS/T on multiorgan EOT.

methodsIn vitro, pulmonary endothelial cell (PEC) and Caco-2 intestinal epithelial cell monolayers were treated with control media, MSC conditioned media (CM), or MSC EVs in varying doses and subjected to a thrombin or hydrogen peroxide (H

resultsMSC EVs and MSC CM attenuated permeability and preserved intercellular junctions of the PEC monolayer in vitro, whereas only MSC CM was protective of the Caco-2 epithelial monolayer. In vivo, both MSC EVs and MSCs mitigated the loss of endothelial adherens junctions in the lung and small intestine, though only MSCs had a protective effect on epithelial tight junctions in the lung. Several plasma biomarkers including MMP8 and VEGF were elevated in LR- and EV-treated but not MSC-treated mice.

conclusionsIn conclusion, MSC EVs could be a potential cell-free therapy targeting endotheliopathy after HS/T via preservation of the vascular endothelial barrier in multiple organs early after injury. Further research is needed to better understand the immunomodulatory effects of these products following HS/T and to move toward translating these therapies into clinical studies.

Indexed as

Extracellular VesiclesMesenchymal Stem CellsMice, Inbred C57BLShock, HemorrhagicAnimalsCaco-2 CellsCulture Media, ConditionedEndothelial CellsEndothelium, VascularHumansHydrogen PeroxideIntercellular JunctionsLungMaleMiceWounds and InjuriesCulture Media, ConditionedHydrogen PeroxideHemorrhagic shockMesenchymal stem cell extracellular vesiclesMesenchymal stem cellsTrauma

Identifiers

PMID38907252
PMCPMC11191310

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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.