ArticleInternational journal of clinical and experimental pathology2018
MicroRNA-124 alleviates hyperoxia-induced inflammatory response in pulmonary epithelial cell by inhibiting TLR4/NF-κB/CCL2.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Androgen Receptor-Controlled microRNA-124-3p.2 Suppresses Prostate Cancer Progression via CCL2 Inhibition.Cancer science · 2025Article
- MicroRNA-214 promotes alveolarization in neonatal rat models of bronchopulmonary dysplasia via the PlGF-dependent STAT3 pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Screening and identification of key regulatory connections and immune cell infiltration characteristics for lung transplant rejection using mucosal biopsies.International immunopharmacology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung epithelial cell dysfunction induced by hyperoxia-associated oxidative stress is a prominent feature involved in the development of acute lung injury (ALI). How the underlying molecular mechanisms contributed to this process are poorly defined. In the present study, we sought to identify the role of miR-124 in hyperoxia-induced cell apoptosis and excessive inflammatory response in pulmonary epithelial cell.
methodsThe miR-124 levels in pulmonary epithelial cell were assayed by qRT-PCR. MiR-124 mimics and inhibitors were transfected to gain or loss of miR-124 function. Cell proliferation was analyzed by CCK8 assay. Cell apoptosis was analyzed by flow cytometry. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The protein levels were assayed by western blotting.
resultsThe results showed that miR-124 was significantly down-regulated in Beas2B cells and primary LECs upon hyperoxia exposure conditions. However, overexpression of miR-124 dramatically attenuated hyperoxia-provoked TLR4, NF-κB and pro-inflammatory cytokines production.
conclusionIt was concluded that miR-124 inhibited hyperoxia-induced apoptosis and excessive inflammatory response in Beas2B cells and primary LECs, at least partially, through the inhibition of TLR4/NF-κB/CCL2 signaling cascades.
Indexed as
Identifiers
31938089PMC6957945W3028010003What OpenQuestion holds
Registered trials
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