Evidence map›Paper›PMID 25310015›Full record

ArticlePloS one2014

Induced pluripotent stem cell therapy ameliorates hyperoxia-augmented ventilator-induced lung injury through suppressing the Src pathway.

Yung-Yang Liu, Li-Fu Li, Jui-Ying Fu, Kuo-Chin Kao, Chung-Chi Huang, Yueh Chien, Yi-Wen Liao, Shih-Hwa Chiou, Yuh-Lih Chang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. 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
3.4field-weighted citation impact, top 8% 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, 31 citations in OpenAlex.

  1. Review
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  11. Ventilator-induced diaphragm dysfunction in critical illness.Experimental biology and medicine (Maywood, N.J.) · 2018
    Review
  12. Article
  13. Developmental pathways in lung regeneration.Cell and tissue research · 2017
    Review
  14. Article
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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

9 authors at 5 institutions in 1 country.

Yung-Yang LiuChest Department, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Li-Fu LiDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan; Department of Respiratory Therapy, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Jui-Ying FuDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan.
Kuo-Chin KaoDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan; Department of Respiratory Therapy, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Chung-Chi HuangDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan; Department of Respiratory Therapy, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Yueh ChienDepartment of Medical Research & Education, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yi-Wen LiaoDepartment of Medical Research & Education, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Shih-Hwa ChiouInstitute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan; Department of Medical Research & Education, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yuh-Lih ChangDepartment of Medical Research & Education, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Chang Gung Memorial Hospital · TWNational Yang Ming Chiao Tung University · TWChang Gung University · TWNational Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh tidal volume (VT) mechanical ventilation (MV) can induce the recruitment of neutrophils, release of inflammatory cytokines and free radicals, and disruption of alveolar epithelial and endothelial barriers. It is proposed to be the triggering factor that initiates ventilator-induced lung injury (VILI) and concomitant hyperoxia further aggravates the progression of VILI. The Src protein tyrosine kinase (PTK) family is one of the most critical families to intracellular signal transduction related to acute inflammatory responses. The anti-inflammatory abilities of induced pluripotent stem cells (iPSCs) have been shown to improve acute lung injuries (ALIs); however, the mechanisms regulating the interactions between MV, hyperoxia, and iPSCs have not been fully elucidated. In this study, we hypothesize that Src PTK plays a critical role in the regulation of oxidants and inflammation-induced VILI during hyperoxia. iPSC therapy can ameliorate acute hyperoxic VILI by suppressing the Src pathway.

methodsMale C57BL/6 mice, either wild-type or Src-deficient, aged between 2 and 3 months were exposed to high VT (30 mL/kg) ventilation with or without hyperoxia for 1 to 4 h after the administration of Oct4/Sox2/Parp1 iPSCs at a dose of 5×10(7) cells/kg of mouse. Nonventilated mice were used for the control groups.

resultsHigh VT ventilation during hyperoxia further aggravated VILI, as demonstrated by the increases in microvascular permeability, neutrophil infiltration, macrophage inflammatory protein-2 (MIP-2) and plasminogen activator inhibitor-1 (PAI-1) production, Src activation, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and malaldehyde (MDA) level. Administering iPSCs attenuated ALI induced by MV during hyperoxia, which benefited from the suppression of Src activation, oxidative stress, acute inflammation, and apoptosis, as indicated by the Src-deficient mice.

conclusionThe data suggest that iPSC-based therapy is capable of partially suppressing acute inflammatory and oxidant responses that occur during hyperoxia-augmented VILI through the inhibition of Src-dependent signaling pathway.

Indexed as

Stem Cell TransplantationAnimalsApoptosisCellular ReprogrammingChemokine CXCL2Enzyme ActivationEpithelial CellsFibroblastsHyperoxiaInduced Pluripotent Stem CellsInflammationLungMaleMembrane GlycoproteinsMice, Inbred C57BLNADPH Oxidase 2Chemokine CXCL2Cybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesOctamer Transcription Factor-3Plasminogen Activator Inhibitor 1Poly(ADP-ribose) PolymerasesPou5f1 protein, mouseReactive Oxygen SpeciesSOXB1 Transcription Factorssrc-Family Kinases

Identifiers

PMID25310015
PMCPMC4195701
OpenAlexW2053560600

What OpenQuestion holds

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LicenceCC BY
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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.