Evidence map›Paper›PMID 38195465›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

IRF4 affects the protective effect of regulatory T cells on the pulmonary vasculature of a bronchopulmonary dysplasia mouse model by regulating FOXP3.

Ying Zhu, Langyue He, Yue Zhu, Huici Yao, Jianfeng Jiang, Hongyan Lu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 2 syntheses or guidelines pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
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 at 1 institution in 1 country.

Ying Zhu *Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Langyue He *Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Yue ZhuDepartment of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Huici YaoDepartment of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Jianfeng JiangDepartment of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Hongyan LuDepartment of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, China. lhy5154@163.com.ORCID 0000-0003-4367-2715
Jiangsu University · CN

Funding

Basic Research Program of Jiangsu Province BK20201226Innovative Research Group Project of the National Natural Science Foundation of China 82171702
6 · The paper itself

Abstract

backgroundBronchopulmonary dysplasia (BPD) is a common chronic lung disease in preterm infants, characterised by compromised alveolar development and pulmonary vascular abnormalities. Emerging evidence suggests that regulatory T cells (Tregs) may confer protective effects on the vasculature. Knockdown of their transcription factor, interferon regulatory factor 4 (IRF4), has been shown to promote vascular endothelial hyperplasia. However, the involvement of Tregs and IRF4 in the BPD pathogenesis remains unclear. This study aimed to investigate the regulation of Tregs by IRF4 and elucidate its potential role in pulmonary vasculature development in a BPD mouse model.

methodsThe BPD model was established using 85% hyperoxia exposure, with air exposure as the normal control. Lung tissues were collected after 7 or 14 days of air or hyperoxia exposure, respectively. Haematoxylin-eosin staining was performed to assess lung tissue pathology. Immunohistochemistry was used to measure platelet endothelial cell adhesion molecule-1 (PECAM-1) level, flow cytometry to quantify Treg numbers, and Western blot to assess vascular endothelial growth factor (VEGFA), angiopoietin-1 (Ang-1), forkhead box protein P3 (FOXP3), and IRF4 protein levels. We also examined the co-expression of IRF4 and FOXP3 proteins using immunoprecipitation and immunofluorescence double staining. Furthermore, we employed CRISPR/Cas9 technology to knock down the IRF4 gene and observed changes in the aforementioned indicators to validate its effect on pulmonary vasculature development in mice.

resultsElevated IRF4 levels in BPD model mice led to FOXP3 downregulation, reduced Treg numbers, and impaired pulmonary vascular development. Knockdown of IRF4 resulted in improved pulmonary vascular development and upregulated FOXP3 level.

conclusionIRF4 may affect the protective role of Tregs in the proliferation of pulmonary vascular endothelial cells and pulmonary vascular development in BPD model mice by inhibiting the FOXP3 level.

Indexed as

Bronchopulmonary DysplasiaHyperoxiaAnimalsDisease Models, AnimalEndothelial CellsForkhead Transcription FactorsHumansInfantInfant, NewbornInfant, PrematureInterferon Regulatory Factor-4Interferon Regulatory FactorsMiceT-Lymphocytes, RegulatoryVascular Endothelial Growth Factor AForkhead Transcription FactorsFOXP3 protein, humanFoxp3 protein, mouseInterferon Regulatory Factor-4Interferon Regulatory FactorsVascular Endothelial Growth Factor ABronchopulmonary dysplasiaForkhead box protein P3Interferon regulatory factor 4Pulmonary vascular developmentPulmonary vascular endothelial cellsRegulatory T cells

Identifiers

PMID38195465
PMCPMC10777489
OpenAlexW4390777528

What OpenQuestion holds

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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.