ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
miR-124 regulates fetal pulmonary epithelial cell maturation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 41 citations in OpenAlex.
- The emerging regulatory roles of non-coding RNA in Ventilator-induced Lung Injury.Non-coding RNA research · 2026Review
- Article
- MicroRNA-124-5p delays the progression of cerebral aneurysm by regulating FoxO1.Experimental and therapeutic medicine · 2021Article
- Lipopolysaccharide Inhibits Alpha Epithelial Sodium Channel Expression via MiR-124-5p in Alveolar Type 2 Epithelial Cells.BioMed research international · 2020Article
- miR-20a-5p regulates pulmonary surfactant gene expression in alveolar type II cells.Journal of cellular and molecular medicine · 2019Article
- MiR-21 improves invasion and migration of drug-resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1.Cancer medicine · 2018Article
- Prognostic significance of NFIA and NFIB in esophageal squamous carcinoma and esophagogastric junction adenocarcinoma.Cancer medicine · 2018Article
- MicroRNA-124 alleviates hyperoxia-induced inflammatory response in pulmonary epithelial cell by inhibiting TLR4/NF-κB/CCL2.International journal of clinical and experimental pathology · 2018Article
- Pri-microRNA-124 rs531564 polymorphism minor allele increases the risk of pulmonary artery hypertension by abnormally enhancing proliferation of pulmonary artery smooth muscle cells.International journal of chronic obstructive pulmonary disease · 2017Article
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- MicroRNA in late lung development and bronchopulmonary dysplasia: the need to demonstrate causality.Molecular and cellular pediatrics · 2016Review
- Transcription Factor NFIB Is a Driver of Small Cell Lung Cancer Progression in Mice and Marks Metastatic Disease in Patients.Cell reports · 2016Article
- Acute cellular rejection elicits distinct microRNA signatures in airway epithelium of lung transplant patients.Transplantation direct · 2015Article
- Dysregulation of non-coding RNAs in gastric cancer.World journal of gastroenterology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
MicroRNAs are a family of small noncoding RNAs that regulate the expression of their target proteins at the posttranscriptional level. Their functions cover almost every aspect of cell physiology. However, the roles of microRNAs in fetal lung development are not completely understood. The objective of this study is to investigate the regulation and molecular mechanisms of alveolar epithelial cell maturation during fetal lung development by miR-124. We discovered that miR-124 was downregulated during rat fetal lung development and predominantly expressed in the epithelial cells at late stage of the lung development. Overexpression of miR-124 with an adenovirus vector led to the inhibition of epithelial maturation in rat fetal lung organ cultures and fetal alveolar epithelial type II cells, as demonstrated by a decrease in the type II cell marker expression and an increase in glycogen content. We further demonstrated by luciferase reporter assays that miR-124 inhibited the NF-κB, cAMP/PKA, and MAPK/ERK pathways. In addition, nuclear factor I/B (NFIB), a critical protein in fetal lung maturation, was validated as a direct target of miR-124. Furthermore, miR-124 expression was induced by the Wnt/β-catenin signaling pathway through a direct interaction of LEF1 and the miR-124 promoter region. We concluded that miR-124 downregulation is critical to fetal lung epithelial maturation and miR-124 inhibits this maturation process at least partially through the inhibition of NFIB.
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