miR-16 inhibits hyperoxia-induced cell apoptosis in human alveolar epithelial cells

  • Authors:
    • Zhixi Li
    • Wenjun Jiang
    • Gang Wu
    • Xueming Ju
    • Youyu Wang
    • Wenying Liu
  • View Affiliations

  • Published online on: February 26, 2018     https://doi.org/10.3892/mmr.2018.8636
  • Pages: 5950-5957
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Abstract

The identification and development of novel therapeutic strategies for acute lung injury is urgently required. It has been previously demonstrated that microRNA (miR)‑16 suppresses the level of transforming growth factor (TGF)‑β in acute lung injury (ALI). Therefore, the present study investigated the role of miR‑16 in the phenotype, cell proliferation and apoptosis, and the involvement of TGF‑β/Smad family member 2 (Smad2) and JAK/signal transducer and activator of transcription (STAT)3 signaling, of primary human alveolar type II epithelial cells (AECII). Following transfection with miR‑16 mimics, AECII cells were exposed to hyperoxia for 24 h. Subsequently, immunofluorescence staining of surfactant protein‑A (SP‑A) was performed, and cell proliferation and apoptosis were investigated by Cell Counting Kit‑8 assays and annexin V‑fluorescein isothiocyanate/propidium iodide staining, respectively. Furthermore, the expression levels of miR‑16, TGF‑β, Smad2, phosphorylated‑Smad2, JAK and STAT3 were detected by western blotting and/or reverse transcription‑quantitative polymerase chain reaction. The results demonstrated that miR‑16 levels and SP‑A fluorescence were markedly inhibited by hyperoxia. Furthermore, transfection of AECII cells with miR‑16 mimics increased SP‑A fluorescence in hyperoxia‑treated AECII cells, significantly reversed hyperoxia‑induced reductions in cell proliferation and inhibited hyperoxia‑induced apoptosis. Finally, miR‑16 mimics modulated the mRNA and protein expression of components of the TGF‑β/Smad2 and JAK/STAT3 pathways in AECII cells following hyperoxia. In conclusion, the results of the present study indicate that overexpression of miR‑16 may exert a protective effect in AECII cells against cell apoptosis and ALI, which may be associated with TGF‑β/Smad2 and JAK/STAT3 signaling pathways. This may also represent a promising target for novel therapeutic strategies for acute lung injury.
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April-2018
Volume 17 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Li Z, Jiang W, Wu G, Ju X, Wang Y and Liu W: miR-16 inhibits hyperoxia-induced cell apoptosis in human alveolar epithelial cells. Mol Med Rep 17: 5950-5957, 2018.
APA
Li, Z., Jiang, W., Wu, G., Ju, X., Wang, Y., & Liu, W. (2018). miR-16 inhibits hyperoxia-induced cell apoptosis in human alveolar epithelial cells. Molecular Medicine Reports, 17, 5950-5957. https://doi.org/10.3892/mmr.2018.8636
MLA
Li, Z., Jiang, W., Wu, G., Ju, X., Wang, Y., Liu, W."miR-16 inhibits hyperoxia-induced cell apoptosis in human alveolar epithelial cells". Molecular Medicine Reports 17.4 (2018): 5950-5957.
Chicago
Li, Z., Jiang, W., Wu, G., Ju, X., Wang, Y., Liu, W."miR-16 inhibits hyperoxia-induced cell apoptosis in human alveolar epithelial cells". Molecular Medicine Reports 17, no. 4 (2018): 5950-5957. https://doi.org/10.3892/mmr.2018.8636