ArticleBioscience reports2020
MiR-124-3p helps to protect against acute respiratory distress syndrome by targeting p65.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- MicroRNAs as Biomarkers for the Diagnosis and Prognosis of Different Diseases and Cancer.Experientia supplementum (2012) · 2026Review
- Function and mechanism of miRNAs during the process ofBiomolecules & biomedicine · 2025Review
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Biomarker potential of competing endogenous RNA networks in Polycystic Ovary Syndrome (PCOS).Non-coding RNA research · 2024Review
- Review
- 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
- The role of microRNAs in nicotine signaling.EXCLI journal · 2023Review
- Article
- Multiple functions of stress granules in viral infection at a glance.Frontiers in microbiology · 2023Review
- Increased miR-124-3p alleviates type 2 inflammatory response in allergic rhinitis via IL-4Rα.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- MicroRNAs: Important Regulatory Molecules in Acute Lung Injury/Acute Respiratory Distress Syndrome.International journal of molecular sciences · 2022Review
- New challenges for microRNAs in acute pancreatitis: progress and treatment.Journal of translational medicine · 2022Review
- Article
- MicroRNAs based regulation of cytokine regulating immune expressed genes and their transcription factors in COVID-19.Meta gene · 2022Article
- miRNAs: The Key Regulator of COVID-19 Disease.International journal of cell biology · 2022Review
- Insights into the SARS-CoV-2-Mediated Alteration in the Stress Granule Protein Regulatory Networks in Humans.Pathogens (Basel, Switzerland) · 2021Article
- The potential role of miR-124-3p in tumorigenesis and other related diseases.Molecular biology reports · 2021Review
- PDE4 inhibition as a therapeutic strategy for improvement of pulmonary dysfunctions in Covid-19 and cigarette smoking.Biochemical pharmacology · 2021Review
- Long non-coding RNA SNHG5 suppresses the development of acute respiratory distress syndrome by targeting miR-205/COMMD1 axis.Molecular and cellular biochemistry · 2021Article
- Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
Corrections and comments
- Expression of concern
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute respiratory distress syndrome (ARDS) is a severe form of acute lung injury that has a high mortality rate and leads to substantial healthcare costs. MicroRNA-124-3p (miR-124-3p) helps to suppress inflammation during a pulmonary injury. However, its mechanism of action is largely unknown, and its role in ARDS remains to be determined.
methodsMice and NR8383 cells were exposed to lipopolysaccharides (LPS) to induce ARDS, and their miR-124-3p levels were determined. After a miRNA agomir was administrated to the mice, their pulmonary injuries were evaluated by H&E staining and assays for peripheral inflammatory cytokine levels. The direct interaction between miR-124-3p and p65 was predicted, and then confirmed by a luciferase activity assay. The role played by miRNA-124-3p in regulating p65 expression was further examined by transfection with its agomir, and its role in cell apoptosis was investigated by observing the effects of miRNA overexpression in vitro and in vivo.
resultsAfter exposure to LPS, there was a consistent decrease in miR-124-3p expression in the lungs of mice and in NR8383 cells. After treatment with the miR-124-3p agomir, the degrees of pulmonary injury (e.g. alveolar hemorrhage and interstitial edema), and the increases in IL-1β, IL-6, and TNF-α levels induced by LPS were significantly attenuated. Overexpression of miR-124-3p in NC8383 cells and lung tissues significantly suppressed LPS-induced p65 expression and cell apoptosis.
conclusionsThese results suggest that miR-124-3p directly targeted p65, and thereby decreased the levels of inflammation and pulmonary injury in a mouse model of ARDS.
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