Evidence map›Paper›PMID 35382387›Full record

ArticleJournal of scleroderma and related disorders2019

Fos-related antigen-1 transgenic mouse as a model for systemic sclerosis: A potential role of M2 polarization.

Hidekata Yasuoka, Yuen Yu Angela Tam, Yuka Okazaki, Yuichi Tamura, Koichi Matsuo, Carol Feghali-Bostwick, Tsutomu Takeuchi, Masataka Kuwana

Open access · greenAbstract read
In one paragraph

Article in Journal of scleroderma and related disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 93% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 2 countries.

Hidekata YasuokaDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Yuen Yu Angela TamDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Yuka OkazakiDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Yuichi TamuraInternational University of Health and Welfare, Mita Hospital, Tokyo, Japan.
Koichi MatsuoLaboratory of Cell and Tissue Biology, School of Medicine, Keio University, Tokyo, Japan.
Carol Feghali-BostwickMedical University of South Carolina, Charleston, SC, USA.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Masataka KuwanaDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.ORCID https://orcid.org/0000-0001-8352-6136
Keio University · JPMedical University of South Carolina · USMita Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: To investigate the systemic sclerosis-related phenotype in fos-related antigen-1 transgenic mice and its underlying mechanisms. Methods: Lung and skin sections of constitutive fos-related antigen-1 transgenic mice and wild-type mice were examined by tissue staining and immunohistochemistry. The tricuspid regurgitation pressure gradient was measured by transthoracic echocardiography with a Doppler technique. To assess the impact of fos-related antigen-1 expression on macrophage function, bone marrow-derived mononuclear cells were derived from mice that expressed fos-related antigen-1 under the control of doxycycline and wild-type littermates. These bone marrow-derived mononuclear cells were induced to differentiate into macrophages with or without doxycycline, and analyzed for gene and protein expression. Finally, lung explants obtained from systemic sclerosis patients and control donors were subjected to immunohistochemistry. Results: The lungs of fos-related antigen-1 transgenic mice showed excessive fibrosis of the interstitium and thickening of vessel walls, with narrowing lumen, in an age-dependent manner. The tricuspid regurgitation pressure gradient was significantly elevated in fos-related antigen-1 transgenic versus control mice. Increased dermal thickness and the loss of subdermal adipose tissue were also observed in the fos-related antigen-1 transgenic mice. These changes were preceded by a perivascular infiltration of mononuclear cells, predominantly consisting of alternatively activated or M2 macrophages. Overexpressing fos-related antigen-1 in bone marrow-derived mononuclear cell cultures increased the expression of M2-related genes, such as Conclusions: The fos-related antigen-1 transgenic mouse serves as a genetic model of systemic sclerosis that recapitulates the major vascular and fibrotic manifestations of the lungs and skin in systemic sclerosis patients. M2 polarization mediated by the up-regulation of fos-related antigen-1 may play a critical role in the development of systemic sclerosis.

Indexed as

Interstitial lung diseasemacrophagesmouse modelpulmonary arterial hypertensionsystemic sclerosis

Identifiers

PMID35382387
PMCPMC8922645
OpenAlexW2946401472

What OpenQuestion holds

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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.