miR-296-5p Inhibits the Secretion of Pulmonary Surfactants in Pulmonary Epithelial Cells via the Downregulation of Wnt7b/ β-Catenin Signaling

Biomed Res Int. 2021 Jan 5:2021:4051504. doi: 10.1155/2021/4051504. eCollection 2021.

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.

MeSH terms

  • A549 Cells
  • Apoptosis / genetics
  • Cell Survival / genetics
  • Down-Regulation / genetics
  • Humans
  • Infant, Newborn
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Pulmonary Surfactants / metabolism*
  • Respiratory Distress Syndrome, Newborn* / genetics
  • Respiratory Distress Syndrome, Newborn* / metabolism
  • Wnt Signaling Pathway / genetics*

Substances

  • MIRN296 microRNA, human
  • MicroRNAs
  • Pulmonary Surfactants