Evidence map›Paper›PMID 36135181›Full record

ArticleCurrent issues in molecular biology2022

Fetal Lung Cells Transfer Improves Emphysematous Change in a Mouse Model of Neutrophil Elastase-Induced Lung Emphysema.

Shin Ohta, Akihiko Tanaka, Tomoko Okazaki, Hatsuko Mikuni, Tomoki Uno, Yoshitaka Uchida, Tomoyuki Kimura, Yosuke Fukuda, Megumi Jinno, Kuniaki Hirai and 6 more

Open access · goldAbstract read
In one paragraph

Article in Current issues in molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 82% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

16 authors at 1 institution in 1 country.

Shin OhtaDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.ORCID 0000-0001-8744-6096
Akihiko TanakaDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Tomoko OkazakiDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Hatsuko MikuniDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Tomoki UnoDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Yoshitaka UchidaDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.ORCID 0000-0002-7269-3956
Tomoyuki KimuraDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Yosuke FukudaDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Megumi JinnoDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Kuniaki HiraiDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Yoshito MiyataDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Hideki InoueDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.ORCID 0000-0002-8624-6524
Tetsuya HommaDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Mayumi YamamotoDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Shintaro SuzukiDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.
Hironori SagaraDepartment of Medicine, Division of Respiratory Medicine and Allergology, Showa University, Tokyo 142-8666, Japan.ORCID 0000-0003-2376-1606
Showa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, several studies for lung regeneration have been reported. However, regenerating the lung tissue by the transfer of any cells directly to the lung has been hardly successful. The aim of this study was to evaluate the effect of fetal lung cells (FLCs) in a mouse model of lung emphysema. C57BL/6 mice were stimulated with neutrophil elastase (NE) intra-tracheally (i.t.) to generate lung emphysema. To collect fetal lung cells, C57BL/6-Tg (CAG-EGFP) mice were bred for 14 days. Before delivery, the bred mice were euthanized, and fetal lungs were harvested from the fetal mice and the cells were collected. The FLCs were transferred i.t. 24 h after the NE instillation. Four weeks after the NE instillation, mice were euthanized, and the samples were collected. The mean linear intercept (MLI) was significantly prolonged in the NE instillation group compared to the control group. However, in the FLCs transfer group stimulated with NE, the MLI became shorter than the NE-stimulated group without an FLCs transfer. This result shows that an FLCs transfer inhibited the progression of lung emphysema. Additionally, motility of the mice was also improved by the FLCs transfer. These results indicate that transfer of the FLCs, which were presumed to be progenitor cells for lung tissue, may improve the emphysematous change.

Indexed as

fetal lung celllung emphysemamouse modelneutrophil elastaseregeneration

Identifiers

PMID36135181
PMCPMC9497467
OpenAlexW4293526679

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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.