ArticleImmunity, inflammation and disease2023
The miR-124-3p regulates the allergic airway inflammation and remodeling in an ovalbumin-asthmatic mouse model by inhibiting S100A4.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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.
Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The Role of Alarmins in the Pathogenesis of Asthma.Biomolecules · 2025Review
- Effects of FAP+ fibroblasts on cell proliferation migration and immunoregulation of esophageal squamous carcinoma cells through the CXCL12/CXCR4 axis.Molecular and cellular biochemistry · 2025Article
- Targeting Lung Damage: Amniotic Mesenchymal Stem Cells Mitigate Lipopolysaccharide-Induced Acute Lung Injury via Multiple Signaling Pathways.International journal of molecular sciences · 2025Article
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs.Frontiers in genetics · 2025Review
- Xuanhong Dingchuan Tang suppresses bronchial asthma inflammation via the microRNA-107-3p/PTGS2/MAPK axis.Functional & integrative genomics · 2024Article
- The miR-9-5p/KLF5/IL-1β Axis Regulates Airway Smooth Muscle Cell Proliferation and Apoptosis to Aggravate Airway Remodeling and Inflammation in Asthma.Biochemical genetics · 2024Article
- The miR-124-3p regulates the allergic airway inflammation and remodeling in an ovalbumin-asthmatic mouse model by inhibiting S100A4.Immunity, inflammation and disease · 2023Article
- Medicine Targeting Epithelial-Mesenchymal Transition to Treat Airway Remodeling and Pulmonary Fibrosis Progression.Canadian respiratory journal · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAsthma is a chronic respiratory disease with an increasing incidence every year. microRNAs (miRNAs) have been demonstrated to have implications for asthma. However, limited information is available regarding the effect of miR-124-3p on this disease. Therefore, this study aimed to explore the possible effects of miR-124-3p and S100A4 on inflammation and epithelial-mesenchymal transition (EMT) in asthma using mouse models.
methodOvalbumin was used to induce asthmatic mouse models. Lung injury in mouse models was assessed, and the bronchoalveolar lavage fluid of mice was collected to determine the number of eosinophilic granulocytes and assess inflammation. The expression levels of miR-124-3p, S100A4, E-cadherin, N-cadherin, Snail1, vimentin, and TGF-β1/Smad2 signaling pathway-related proteins were measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. In vitro experiments, cells were transfected with miR-124-3p mimics or inhibitors to test the expression of S100A4 by RT-qPCR and western blot analysis, and the mutual binding of miR-124-3p and S100A4 was validated by dual-luciferase reporter gene assay.
resultsOverexpression of miR-124-3p or inhibition of S100A4 expression attenuated bronchial mucus secretion and collagenous fibers and suppressed inflammatory cell infiltration. Additionally, upon miR-124-3p overexpression or S100A4 suppression, eosinophilic granulocytes were decreased, interleukin-4 (IL-4) and IL-13 expression levels were reduced in the bronchoalveolar lavage fluid, serum total IgE level was reduced, and the TGF-β1/Smad2 signaling pathway was suppressed. Mechanically, a dual-luciferase reporter gene assay verified the binding relationship between miR-124-3p and S100A4.
conclusionmiR-124-3p can negatively target S100A4 to attenuate inflammation in asthmatic mouse models by suppressing the EMT process and the TGF-β/smad2 signaling pathway.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.