Evidence map›Paper›PMID 33246503›Full record

ArticleStem cell research & therapy2020

Exosomes from adipose tissue-derived mesenchymal stem cells ameliorate histone-induced acute lung injury by activating the PI3K/Akt pathway in endothelial cells.

Yukie Mizuta, Tomohiko Akahoshi, Jie Guo, Shuo Zhang, Sayoko Narahara, Takahito Kawano, Masaharu Murata, Kentaro Tokuda, Masatoshi Eto, Makoto Hashizume and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.8field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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  20. Translational medicine for acute lung injury.Journal of translational medicine · 2024
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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

11 authors at 1 institution in 1 country.

Yukie MizutaDepartment of Disaster and Emergency Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Tomohiko AkahoshiDepartment of Disaster and Emergency Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. tomohiko@dem.med.kyushu-u.ac.jp.ORCID 0000-0002-1750-2299
Jie GuoDepartment of Disaster and Emergency Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Shuo ZhangDepartment of Disaster and Emergency Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Sayoko NaraharaCenter for Advanced Medical Innovation, Kyushu University, Fukuoka, Japan.
Takahito KawanoCenter for Advanced Medical Innovation, Kyushu University, Fukuoka, Japan.
Masaharu MurataCenter for Advanced Medical Innovation, Kyushu University, Fukuoka, Japan.
Kentaro TokudaDepartment of Anesthesiology and Critical Care Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Masatoshi EtoCenter for Advanced Medical Innovation, Kyushu University, Fukuoka, Japan.
Makoto HashizumeCenter for Advanced Medical Innovation, Kyushu University, Fukuoka, Japan.
Ken YamauraDepartment of Anesthesiology and Critical Care Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesenchymal stem cells (MSCs), including adipose-derived mesenchymal stem cells (ADSCs), have been shown to attenuate organ damage in acute respiratory distress syndrome (ARDS) and sepsis; however, the underlying mechanisms are not fully understood. In this study, we aimed to explore the potential roles and molecular mechanisms of action of ADSCs in histone-induced endothelial damage.

methodsMale C57BL/6 N mice were intravenously injected with ADSCs, followed by histones or a vehicle. The mice in each group were assessed for survival, pulmonary vascular permeability, and histological changes. A co-culture model with primary human umbilical vein endothelial cells (HUVECs) exposed to histones was used to clarify the paracrine effect of ADSCs. Overexpression and inhibition of miR-126 ADSCs were also examined as causative factors for endothelial protection.

resultsThe administration of ADSCs markedly improved survival, inhibited histone-mediated lung hemorrhage and edema, and attenuated vascular hyper-permeability in mice. ADSCs were engrafted in the injured lung and attenuated histone-induced endothelial cell apoptosis. ADSCs showed endothelial protection (via a paracrine effect) and Akt phosphorylation in the histone-exposed HUVECs. Notably, increased Akt phosphorylation by ADSCs was mostly mediated by exosomes in histone-induced cytotoxicity and lung damage. Moreover, the expression of miR-126 was increased in exosomes from histone-exposed ADSCs. Remarkably, the inhibition of miR-126 in ADSCs failed to increase Akt phosphorylation in histone-exposed HUVECs.

conclusionADSC-derived exosomes may exert protective effects on endothelial cells via activation of the PI3K/Akt pathway.

Indexed as

Acute Lung InjuryExosomesMesenchymal Stem CellsAdipose TissueAnimalsHistonesMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktHistonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAcute lung injuryAcute respiratory distress syndromeAdipose-derived mesenchymal stem cellsEndothelial damageExosomesHistonesmiR-126PI3K/Akt signaling pathwaySepsis

Identifiers

PMID33246503
PMCPMC7691956
OpenAlexW3106620956

What OpenQuestion holds

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LicenceCC BY
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.