Background: Neonatal pneumonia is a common disease in the neonatal period with a
high incidence and death. This study aimed to investigate the molecular mechanism and effect of
microRNA (miR)-429 in neonatal pneumonia.
Methods: The peripheral blood was collected from neonatal pneumonia and healthy patients,
respectively. Human lung fibroblast WI-38 cells were treated with lipopolysaccharide (LPS) to
establish neonatal pneumonia cell model. Then, the miR-429 expression was detected by quantitative
real-time polymerase chain reaction (qRT-PCR). In addition, the relationship between miR-
429 and kruppel-like factor 4 (KLF4) was confirmed by dual luciferase reporter assay. Cell viability,
the level of interleukin 6 (IL-6), IL-1β and tumor necrosis factor α (TNF-α) and apoptosis were
measured by Cell Counting Kit-8 (CCK-8), enzyme linked immunosorbent assay (ELISA) and
flow cytometry. Meanwhile, apoptosis and nuclear factor kappa-B (NF-κB) pathway related proteins
expression were analyzed by western blot.
Results: MiR-429 expression level was increased in neonatal peripheral blood and LPS-stimulated
WI-38 cells. Then, miR-429 overexpression increased apoptosis, the level of IL-6, IL-1β, TNF-α,
Bax and cleaved caspase-3, while reduced cell viability in LPS-stimulated WI-38 cells. Besides,
KLF4 was identified as the target gene of miR-429, and reversed the changes caused by miR-429
overexpression. Finally, miR-429 suppressor down-regulated p-NF-κB level in LPS-stimulated
cells and KLF4 knockdown reversed these reductions.
Conclusion: MiR-429 promotes inflammatory injury, apoptosis and activates the NF-κB signaling
pathway by targeting KLF4 in neonatal pneumonia, and then these results provide evidence for
clinical diagnosis and treatment for neonatal pneumonia.