Evidence map›Paper›PMID 35115789›Full record

ArticleJournal of asthma and allergy2022

Adipose-Derived Mesenchymal Stem Cell-Derived Exosomal miR-301a-3p Regulates Airway Smooth Muscle Cells During Asthma by Targeting STAT3.

Chen-Ye Feng, Shi-Yao Bai, Meng-Lu Li, Jie-Yu Zhao, Jia-Min Sun, Hui-Jing Bao, Yuan Ren, Xin-Ming Su

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of asthma and allergy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  12. Asthma and stem cell therapy.World journal of stem cells · 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

8 authors.

Chen-Ye Feng *Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Shi-Yao Bai *Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Meng-Lu LiDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Jie-Yu ZhaoDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Jia-Min SunDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Hui-Jing BaoDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Yuan RenDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.
Xin-Ming SuDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, The First Affiliated Hospital of China Medical University; Respiratory Disease Institution of China Medical University, Shenyang, Liaoning, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAsthma is a chronic inflammatory disease featured by inflammation and remodeling of airway. Adipose-derived mesenchymal stem cell (ADSCs)-derived exosomal miRNAs have been suggested as promising therapeutic manners for diseases.

methodsADSCs and airway smooth muscle cells (ASMCs) were isolated from SD rats. Flow cytometry was conducted to detect the surface biomarkers of isolated cells. Exosomes were extracted by sequentially centrifuge method and identified by Western blotting and nanoparticle tracking analysis (NTA). Uptake of exosomes by ASMCs was detected by confocal assay. ASMCs were treated with platelet-derived growth factor-BB (PDGF-BB) to mimic cell remodeling and inflammation. Cell counting 8 (CCK-8), Transwell, and flow cytometry were performed to determine the viability, migration, and apoptosis of ASMCs. Release of inflammatory factors was detected by enzyme-linked immunosorbent assay (ELISA). Levels of RNAs and proteins were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. Interaction between miR-301a-3p and signal transducer and activator of transcription 3 (STAT3) was determined by luciferase reporter gene assay. The effect of Exosomal miR-301a-3p was analyzed in ovalbumin (OVA)-induced asthma mouse model.

resultsADSCs-derived exosomes could be effectively internalized by ASMCs. Exosomal miR-301a-3p notably suppressed the PDGF-BB-stimulated proliferation and migration of ASMCs, and enhanced apoptosis, as well as decreased the secretion of inflammatory factors. MiR-301a-3p directly targeted the 3'UTR region of STAT3. STAT3 overexpression reversed the suppressive effects of exosomal miR-301a-3p on ASMCs under PDGF-BB stimulation. The expression of miR-301a-3p and STAT3 was negative correlation in specimen from patients with asthma. Exosomal miR-301a-3p inhibited OVA-induced lung injury by targeting STAT3 in mice.

conclusionThis study exposed that exosomal miR-301a-3p from ADSCs could effectively alleviate PDGF-BB-stimulated remodeling and inflammation of ASMCs via targeting STAT3, presented ADSCs-derived exosomal miR-301a-3p as a promising therapeutic approach for asthma.

Indexed as

asthmaexosomemesenchymal stem cellmiR-301a-3pSTAT3

Identifiers

PMID35115789
PMCPMC8806053

What OpenQuestion holds

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Registered trials

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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.