| Literature DB >> 33490270 |
Ying-Hui Zhang1, Ai-Ling Chen2, Ren-Qiang Yu1, Bei-Bei Jia1, Dan-Ni Ye1, Min Wang1, Ying-Zi Mei1, Guang-Dong Fang1, Shan-Yu Jiang1, Qin Zhou1, Bing Zhang3.
Abstract
Neonatal respiratory distress syndrome (NRDS) is a common disease that occurs in premature infants. However, the mechanisms underlying the disease remain unclear. microRNAs (miRNAs) have been indicated to play a crucial role in the development of NRDS. In this study, we aimed to explore the regulatory mechanisms of miR-296-5p in NRDS. The expression levels of miR-296-5p in preterm infants with NRDS were determined using quantitative reverse-transcription polymerase chain reaction (RT-qPCR). A549 cells were transfected with lentiviral vectors encoding miR-296-5p, and the transfection efficiency was determined using RT-qPCR. Flow cytometry and CCK8 assay were performed to measure apoptosis and proliferation of A549 cells, respectively. The protein levels of pulmonary surfactant SP-A (SFTPA1), SP-B, Wnt7b, and β-catenin were measured using western blotting. We demonstrated an upregulation of miR-296-5p in NRDS. The miR-296-5p was successfully overexpressed in A549 cells via lentivirus transfection, and the upregulation of miR-296-5p inhibited cell proliferation and secretion of SP-A and SP-B and also induced downregulation of the Wnt7b/β-catenin in vitro. Therefore, miR-296-5p inhibits cell proliferation and secretion of pulmonary surfactants in A549 cells via downregulation of Wnt7b/β-catenin signaling.Entities:
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Year: 2021 PMID: 33490270 PMCID: PMC7803427 DOI: 10.1155/2021/4051504
Source DB: PubMed Journal: Biomed Res Int Impact factor: 3.411