Evidence map›Paper›PMID 40905627›Full record

ArticleThe FEBS journal2025

PU.1 and TGF-β signaling activate the cell-surface expression of CD103 in mast cells and dendritic cells: opposite roles of GATA2 in the expression of mucosal mast cell genes.

Kenta Ishii, Kazuki Nagata, Niya Yamashita, Yuki Yamazaki, Yuta Akimoto, Weiting Zhao, Mariko Inoue, Naoto Ito, Kazumi Kasakura, Chiharu Nishiyama

Abstract read
In one paragraph

Article in The FEBS journal, 2025. 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
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.

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

10 authors.

Kenta IshiiDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0009-0002-5696-766X
Kazuki NagataDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0000-0002-0100-4199
Niya YamashitaDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0009-0007-2606-7579
Yuki YamazakiDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0009-0008-8160-0396
Yuta AkimotoDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Weiting ZhaoDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0009-0005-6816-3863
Mariko InoueDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Naoto ItoDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0000-0002-6318-114X
Kazumi KasakuraDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.
Chiharu NishiyamaDepartment of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo, 125-8585, Japan.ORCID https://orcid.org/0000-0002-4082-9097

Funding

Japan Society for the Promotion of Science 20H02939Japan Society for the Promotion of Science 21J12113Japan Society for the Promotion of Science 23H02167Japan Society for the Promotion of Science 23K26860Japan Society for the Promotion of Science 24K17872
6 · The paper itself

Abstract

Mucosal mast cells (MMCs) are distinguished from connective tissue mast cells (MCs) by the specific cell-surface expression of integrin CD103 (also known as integrin αE/β7; αE is encoded by Itgae) and mast cell protease 1 and 2 (Mcpt1 and Mcpt2, respectively). Although the expression of the Mcpt1 and Mcpt2 genes is cooperatively regulated by the transcription factor GATA-binding protein 2 (GATA2) and transforming growth factor beta (TGF-β) signaling in MMCs, the transcriptional mechanism of the cell-surface expression of CD103 remains unknown. We herein found that surface CD103 and Itgae mRNA levels were significantly increased by the knockdown (KD) of Gata2 in mouse bone marrow-derived MCs (BMMCs), which was accelerated by TGF-β stimulation. Since the mRNA levels of Spi1 (encoding transcription factor PU.1) were increased in Gata2 KD BMMCs, we examined the effects of PU.1 on the cell-surface expression of CD103. As expected, CD103 levels on BMMCs were significantly decreased by Spi1 KD and increased by Spi1 overexpression. Spi1 KD suppressed Itgae expression even in the presence of TGF-β in BMMCs and peritoneal MCs, whereas Gata2 KD amplified the TGF-β-induced increase in Itgae expression. The amount of PU.1 binding to the cis-element in the Itgae gene was significantly and moderately increased by Gata2 KD and TGF-β stimulation, respectively. Since PU.1 is an essential transcription factor for dendritic cells (DCs), we examined the role of PU.1 in CD103 cell-surface expression on DCs. The KD experiment using bone marrow-derived DCs (BMDCs) showed a significant decrease in CD103 levels in Spi1-siRNA-transfected BMDCs. We concluded that PU.1 affected CD103 expression on MMCs and DCs by transactivating the Itgae gene, and also that GATA2, which positively regulated the MMC-specific expression of Mcpt1 and Mcpt2, inhibited the cell-surface expression of CD103 by repressing PU.1.

Indexed as

Antigens, CDDendritic CellsGATA2 Transcription FactorIntegrin alpha ChainsMast CellsProto-Oncogene ProteinsTrans-ActivatorsTransforming Growth Factor betaAnimalsCells, CulturedGene Expression RegulationMiceMice, Inbred C57BLProto-Oncogene Protein Spi-1Signal Transductionalpha E integrinsAntigens, CDGata2 protein, mouseGATA2 Transcription FactorIntegrin alpha ChainsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTransforming Growth Factor betaCD103GATA2mast cell proteasePU.1TGF‐β

Identifiers

PMID40905627
PMCPMC12631159

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.