Evidence map›Paper›PMID 23967196›Full record

ArticlePloS one2013

Human mesenchymal stem cells suppress the stretch-induced inflammatory miR-155 and cytokines in bronchial epithelial cells.

Yi-Chun Kuo, Yi-Shuan Julie Li, Jing Zhou, Yu-Ru Vernon Shih, Marina Miller, David Broide, Oscar Kuang-Sheng Lee, Shu Chien

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 29 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

8 authors at 5 institutions in 2 countries.

Yi-Chun KuoInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Yi-Shuan Julie Li
Jing Zhou
Yu-Ru Vernon Shih
Marina Miller
David Broide
Oscar Kuang-Sheng Lee
Shu Chien
University of California, San Diego · USLa Jolla Bioengineering Institute · USNational Yang Ming Chiao Tung University · TWNational Yang Ming University Hospital · TWTaipei Veterans General Hospital · TW

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
Systems Biology Analyses for Hemodynamic Regulation of Vascular HomeostasisR01HL108735 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2012 to 2024
$13.4M
Shear Regulation of MicroRNA Transportomes and Targetomes in Vascular HomeostasisR01HL106579 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2011 to 2022
$8.3M
Eosinophil trafficking and chronic tissue damage induced by allergic inflammationR37AI038425 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2007 to 2016
$3.7M
Eosinophil TraffickingR01AI038425 · NIAID · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI BROIDE, DAVID H · 1996 to 2005
$1.8M
Siglec-F and Resolution of Allergic InflammationR01AI072115 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2008 to 2012
$1.7M
NHLBI NIH HHS HL106579NHLBI NIH HHS HL108735NHLBI NIH HHS R01 HL106579NHLBI NIH HHS R01 HL108735NIAID NIH HHS AI 38425NIAID NIH HHS AI 70535NIAID NIH HHS AI 72115NIAID NIH HHS R01 AI038425NIAID NIH HHS R01 AI072115NIAID NIH HHS R37 AI038425NIAID NIH HHS U19 AI070535
6 · The paper itself

Abstract

Current research in pulmonary pathology has focused on inflammatory reactions initiated by immunological responses to allergens and irritants. In addition to these biochemical stimuli, physical forces also play an important role in regulating the structure, function, and metabolism of the lung. Hyperstretch of lung tissues can contribute to the inflammatory responses in asthma, but the mechanisms of mechanically induced inflammation in the lung remain unclear. Our results demonstrate that excessive stretch increased the secretion of inflammatory cytokines by human bronchial epithelial cells (hBECs), including IL-8. This increase of IL-8 secretion was due to an elevated microRNA-155 (miR-155) expression, which caused the suppression of Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1) production and the subsequent activation of JNK signaling. In vivo studies in our asthmatic mouse model also showed such changes in miR-155, IL-8, and SHIP1 expressions that reflect inflammatory responses. Co-culture with human mesenchymal stem cells (hMSCs) reversed the stretch-induced hBEC inflammatory responses as a result of IL-10 secretion by hMSCs to down-regulate miR-155 expression in hBECs. In summary, we have demonstrated that mechanical stretch modulates the homeostasis of the hBEC secretome involving miR-155 and that hMSCs can be used as a potential therapeutic approach to reverse bronchial epithelial inflammation in asthma.

Indexed as

AnimalsAsthmaBronchiCell LineCoculture TechniquesCytokinesDisease Models, AnimalGene ExpressionHumansInflammationInflammation MediatorsInositol Polyphosphate 5-PhosphatasesLungMechanical PhenomenaMesenchymal Stem CellsMiceCytokinesInflammation MediatorsInositol Polyphosphate 5-PhosphatasesINPP5D protein, humanInpp5d protein, mouseMicroRNAsMIRN155 microRNA, humanOvalbuminPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester Hydrolases

Identifiers

PMID23967196
PMCPMC3742760
OpenAlexW2086392089

What OpenQuestion holds

Textmetadata
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.