Evidence map›Paper›PMID 27270966›Full record

ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2016

Periostin Deficiency Causes Severe and Lethal Lung Injury in Mice With Bleomycin Administration.

Hirofumi Kondoh, Takashi Nishiyama, Yoshinao Kikuchi, Masashi Fukayama, Mitsuru Saito, Isao Kii, Akira Kudo

Open access · bronzeAbstract read
In one paragraph

Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Observational
  2. Periostin function in communication with extracellular matrices.Journal of cell communication and signaling · 2018
    Review
  3. Introductory review: periostin-gene and protein structure.Cellular and molecular life sciences : CMLS · 2017
    Review
  4. Review
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

7 authors at 3 institutions in 1 country.

Hirofumi KondohDepartment of Biological Information, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, Japan (HK, TN, IK, AK)
Takashi NishiyamaDepartment of Biological Information, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, Japan (HK, TN, IK, AK)
Yoshinao KikuchiDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan (YK, MF)
Masashi FukayamaDepartment of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan (YK, MF)
Mitsuru SaitoDepartment of Orthopaedic Surgery, Jikei University School of Medicine, Tokyo, Japan (MS)
Isao KiiDepartment of Biological Information, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, Japan (HK, TN, IK, AK)
Akira KudoDepartment of Biological Information, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama, Japan (HK, TN, IK, AK)
The University of Tokyo · JPTokyo Institute of Technology · JPJikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary capillary leakage followed by influx of blood fluid into the air space of lung alveoli is a crucial step in the progression of acute lung injury (ALI). This influx is due to increased permeability of the alveolar-capillary barrier. The extracellular matrix (ECM) between the capillary and the epithelium would be expected to be involved in prevention of the influx; however, the role of the ECM remains to be addressed. Here, we show that the ECM architecture organized by periostin, a matricellular protein, plays a pivotal role in the survival of bleomycin-exposed mice. Periostin was localized in the alveolar walls. Although periostin-null mice displayed no significant difference in lung histology and air-blood permeability, they exhibited early lethality in a model of bleomycin-induced lung injury, compared with their wild-type counterparts. This early lethality may have been due to increased pulmonary leakage of blood fluid into the air space in the bleomycin-exposed periostin-null mice. These results suggest that periostin in the ECM architecture prevents pulmonary leakage of blood fluid, thus increasing the survival rate in mice with ALI. Thus, this study provides an evidence for the protective role of the ECM architecture in the lung alveoli.

Indexed as

BleomycinAcute Lung InjuryAlternative SplicingAnimalsCell Adhesion MoleculesCollagenExtracellular MatrixLungMiceMice, Inbred C57BLMice, KnockoutPulmonary AlveoliBleomycinCell Adhesion MoleculesCollagenPostn protein, mouseacute lung injuryalveolusbleomycincollagenextracellular matrixfibronectinmatricellularperiostinpulmonary leakagestroma

Identifiers

PMID27270966
PMCPMC4931763
OpenAlexW2417998938

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.