Evidence map›Paper›PMID 40057631›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025

Peroxisome proliferator-activated receptor gamma prevents activation of RBL-2H3 cells by inhibiting FcεRI-mediated signal transduction.

Yu Zhang, Suyu Ruan, Yuhang Xie, Xiaoqing Rui, Jianjun Zhou, Weihua Wang

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. 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
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.

  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

6 authors.

Yu Zhang *Department of Otolaryngology-Head and Neck Surgery, Shanghai East Hospital, School of Medicine, Tongji University, 150 Jimo Road, Shanghai, 200120, China.
Suyu Ruan *Department of Otolaryngology-Head and Neck Surgery, Shanghai East Hospital, School of Medicine, Tongji University, 150 Jimo Road, Shanghai, 200120, China.
Yuhang XieDepartment of Otolaryngology-Head and Neck Surgery, Shanghai Pudong New Area Gongli Hospital, Shanghai, 200120, China.
Xiaoqing RuiDepartment of Otolaryngology-Head and Neck Surgery, Shanghai East Hospital, School of Medicine, Tongji University, 150 Jimo Road, Shanghai, 200120, China.
Jianjun ZhouCancer Stem Cell Institute, Research Center for Translational Medicine, Shanghai East Hospital, School of Medicine, Tongji University, 150 Jimo Road, Shanghai, 200120, China. zhoujj_2000@aliyun.com.
Weihua WangDepartment of Otolaryngology-Head and Neck Surgery, Shanghai East Hospital, School of Medicine, Tongji University, 150 Jimo Road, Shanghai, 200120, China. whwangcn@tongji.edu.cn.

Funding

Shanghai East Hospital Reserve Personnel Training Program 2019YHRCJH02Shanghai Municipal Health Commission Clinical Research Special Project 202150005
6 · The paper itself

Abstract

backgroundMast cells are essential contributors to the pathophysiology of allergic diseases. Peroxisome proliferator-activated receptor gamma (PPAR-γ) has recently been identified as being involved in the anti-inflammatory response by inhibiting mast cell activation.

methodIn this study, the PPAR-γ agonist pioglitazone (PIO) was employed to evaluate the effects of PPAR-γ on the degranulation and production of pro-inflammatory mediators in RBL-2H3 cells. Meanwhile, differentially expressed genes (DEGs) were characterised in mast cells exposed to PIO, and pathway enrichment analysis were conducted. Furthermore, we conducted validation to confirm the involvement of PPAR-γ signaling pathways in the FcεRI-mediated signal transduction in mast cells.

resultsAdministration of PIO significantly reduced the release of β-hexosaminidase and the mRNA expression levels of pro-inflammatory cytokines induced by the cross-linking of FcεRIs expressed on the surface of RBL-2H3 cells. A total of 24 DEGs were identified between RBL-2H3 cells treated with and without PIO, and there were 15 up-regulated and 9 down-regulated. GO and KEGG analyses revealed that the immune system, signal transduction, infectious disease, and signaling molecules and interactions were the most enriched annotations. According to PPI network analysis, most DEGs interacted with PPAR-γ. PPAR-γ agonist could activate PPAR-γ and NRF2 signaling pathways in resting RBL-2H3 cells. The protein expression levels of PPAR-γ, Cpt1a, and Acsl4 were greatly upregulated in activated RBL-2H3 cells mediated by FcεRI aggregation. Moreover, the suppressive effects of PPAR-γ agonist on degranulation and phosphorylation levels of FcεRI-mediated signaling molecules in RBL-2H3 cells were PPAR-γ-dependent.

conclusionThese data demonstrate that PPAR-γ inhibits FcεRI-mediated mast cell activation by modulating intracellular-specific signal transduction in a PPAR-γ-dependent manner.

Indexed as

Mast CellsPioglitazonePPAR gammaReceptors, IgEAnimalsbeta-N-AcetylhexosaminidasesCell DegranulationCell LineCytokinesRatsSignal Transductionbeta-N-AcetylhexosaminidasesCytokinesPioglitazonePPAR gammaReceptors, IgEAllergic inflammationFcεRIMast cellPPAR-γSignal transduction

Identifiers

PMID40057631

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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.