ArticleHistochemistry and cell biology2023
MicroRNA-598 inhibition ameliorates LPS-induced acute lung injury in mice through upregulating Ebf1 expression.
Article in Histochemistry and cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Targeting of miR-93-5p/Mfn2 Axis Attenuates Lung Fibrosis in Rats With Acute Respiratory Distress Syndrome by Regulating Endoplasmic Reticulum Stress.Physiological research · 2025Article
- Neutrophil-derived Il1r2 modulates inflammation and alleviates acute lung injury by promoting M2 macrophage polarization.Scientific reports · 2025Article
- Circulating extracellular vesicles as potential biomarkers and mediators of acute respiratory distress syndrome in sepsis.Scientific reports · 2025Article
- Identification of endothelial and mesenchymal FOXF1 enhancers involved in alveolar capillary dysplasia.Nature communications · 2024Article
- MiR-202-3p Targets Calm1 and Suppresses Inflammation in a Mouse Model of Acute Respiratory Distress Syndrome.Cell biochemistry and biophysics · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Acute lung injury is a critical acute respiratory distress syndrome (ARDS) with high morbidity and mortality. MicroRNAs (miRNAs) have been demonstrated to play important roles regulating acute lung injury development. In this study, we found that the expression of miR-598 was significantly upregulated in the lung tissues of mice with lipopolysaccharide (LPS)-induced acute lung injury. Both loss-of-function and gain-of-function studies were performed to evaluate the function of miR-598 in acute lung injury. The results showed that inhibition of miR-598 attenuated inflammatory response, oxidative stress, and lung injury in mice treated with LPS, while overexpression of miR-598 exacerbated the LPS-induced acute lung injury. Mechanistically, transcription factor Early B-cell Factor-1 (Ebf1) was predicted and validated as a downstream target of miR-598. Overexpression of Ebf1 attenuated LPS-induced production of inflammatory cytokine TNF-α and IL-6, ameliorated LPS-induced oxidative stress, promoted proliferation, and inhibited apoptosis in murine lung epithelial-15 (MLE-15) cells. Moreover, we demonstrated that Ebf1 knockdown abolished the protective effect of miR-598 inhibition in LPS-treated MLE-15 cells. In summary, miR-598 inhibition ameliorates LPS-induced acute lung injury in mice through upregulating Ebf1 expression, which might provide potential therapeutic treatment for acute lung injury.
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