Evidence map›Paper›PMID 32111211›Full record

ArticleRespiratory research2020

HDAC8 inhibitor attenuates airway responses to antigen stimulus through synchronously suppressing galectin-3 expression and reducing macrophage-2 polarization.

Meng-Lu Li, Xin-Ming Su, Yuan Ren, Xuan Zhao, Ling-Fei Kong, Jian Kang

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Application of 18Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  2. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
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  16. Airway hyperresponsiveness development and the toxicity of PM2.5.Environmental science and pollution research international · 2021
    Review
  17. Article
  18. 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.

Meng-Lu LiDepartment of Respiratory and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China.
Xin-Ming SuDepartment of Respiratory and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China.
Yuan RenDepartment of Respiratory and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China.
Xuan ZhaoDepartment of Respiratory and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China.
Ling-Fei KongDepartment of Respiratory and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China.
Jian KangDepartment of Respiratory and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China. kangjian58@163.com.ORCID http://orcid.org/0000-0003-0556-1088
First Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China 81770021Natural Science Foundation of Liaoning Province 201701664
6 · The paper itself

Abstract

backgroundThis study was to investigate of the mechanism by which histone deacetylase (HDAC) 8 inhibitor ameliorated airway hyperresponsiveness (AHR) and allergic airway inflammation.

methodsMice were sensitized and then treated with budesonide (BUD) or PCI-34051 (PCI) prior to exposing to normal saline (NS) or ovalbumin (OVA). The raw264.7 cells were treated with interleukin (IL)-4 and PCI or shRNA alone. Repetitive measurements of enhanced pause (Penh) were executed by increasing concentrations of acetyl-β-methacholine chloride (0 - 50 mg/ml). Cells in bronchoalveolar lavage fluid (BALF) and pathological changes of lungs were examined, respectively. The expression levels of HDAC8, Galecitn (Gal)-3, CD68, CD86, CD163, Arg1 and NOS2 in lungs were measured. Co-regulation of HDAC8 and Gal-3 proteins was observed by immunofluorescence staining and co-immunoprecipitation assay (Co-IP).

resultsSignificant increases in Penh and IL-4 level were detected with a large inflammatory infiltrate, comprised predominantly of macrophages and eosinophils, into the BALF in OVA-exposed lungs. HDAC8, Gal-3, CD68, CD86, CD163, Arg1 and NOS2 proteins were over-expressed with the significant changes in the Arg1 and NOS2 mRNA levels in the lungs and the IL-4-treated cells. PCI intervention obviously reduced the counts of CD163

conclusionsThe HDAC8 inhibitor ameliorates AHR and airway inflammation in animal model of allergic asthma through reducing HDAC8-Gal-3 interaction and M2 macrophage polarization.

Indexed as

AnimalsBronchial HyperreactivityCell PolarityFemaleGalectin 3Histone DeacetylasesHydroxamic AcidsIndolesLungMacrophagesMiceMice, Inbred BALB COvalbuminRandom AllocationRAW 264.7 CellsGalectin 3HDAC8 protein, mouseHistone DeacetylasesHydroxamic AcidsIndolesLgals3 protein, mouseOvalbuminPCI 34051Galectin-3Histone deacetylases8M2 macrophage polarizationPCI-34051

Identifiers

PMID32111211
PMCPMC7048058
OpenAlexW3012367931

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.