Evidence map›Paper›PMID 30654796›Full record

ArticleRespiratory research2019

Loss of the adhesion G-protein coupled receptor ADGRF5 in mice induces airway inflammation and the expression of CCL2 in lung endothelial cells.

Fumimasa Kubo, Donna Maretta Ariestanti, Souta Oki, Taku Fukuzawa, Ryotaro Demizu, Tomoya Sato, Rahmaningsih Mara Sabirin, Shigehisa Hirose, Nobuhiro Nakamura

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
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  5. Patterns and Processes of Genomic Evolution Inferred From the Ten Smallest Vertebrate Genomes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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 1 institution in 2 countries.

Fumimasa KuboDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Donna Maretta AriestantiDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Souta OkiDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Taku FukuzawaDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Ryotaro DemizuDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Tomoya SatoDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Rahmaningsih Mara SabirinDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Shigehisa HiroseDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan.
Nobuhiro NakamuraDepartment of Life Science and Technology, Tokyo Institute of Technology, 4259-B13 Nagatsuta-cho, Midori-ku, Yokohama, 226-8501, Japan. nnakamur@bio.titech.ac.jp.ORCID http://orcid.org/0000-0002-0249-2665
Tokyo Institute of Technology · JP

Funding

Japan Society for the Promotion of Science 16K07344
6 · The paper itself

Abstract

backgroundAdhesion G-protein coupled receptor F5 (ADGRF5) was recently identified as an essential regulator of pulmonary surfactant homeostasis in alveolar type II cells. We previously showed that in addition to abnormal surfactant accumulation, Adgrf5-deficient (Adgrf5

methodsHistological features of lungs were evaluated by Alcian blue and Masson's trichrome staining. Quantitative real-time PCR (qPCR) and western blot analyses were performed to analyze the differential expression of genes/proteins related to airway inflammation in lungs between wildtype and Adgrf5

resultsAdgrf5

conclusionsTargeted disruption of ADGRF5 results in the development of airway inflammation, which is likely mediated by the type 2 immune response and possibly CCL2-mediated inflammation. ADGRF5 also has a potential role in the regulation of genes encoding CCL2 in lung ECs, thereby maintaining immune homeostasis.

Indexed as

AnimalsBronchitisChemokine CCL2Endothelial CellsGene ExpressionHumansInflammation MediatorsLungMiceMice, Inbred C57BLMice, KnockoutReceptors, G-Protein-CoupledCcl2 protein, mouseChemokine CCL2Gpr116 protein, mouseInflammation MediatorsReceptors, G-Protein-CoupledAdhesion GPCRAsthmaCOPDEndothelial cellFibrosisGPR116Ig-HeptaMucous cell metaplasiaType 2 cytokine

Identifiers

PMID30654796
PMCPMC6337809
OpenAlexW2914017661

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.