ABSTRACT
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-1ß 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-1ß, 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.
Subject(s)
Kruppel-Like Transcription Factors/metabolism , Lung/metabolism , MicroRNAs/metabolism , Pneumonia/blood , Apoptosis/physiology , Cell Survival/physiology , Female , Humans , Infant, Newborn , Inflammation , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Kruppel-Like Factor 4 , Lipopolysaccharides/pharmacology , Lung/cytology , Lung/drug effects , Male , NF-kappa B/metabolism , Tumor Necrosis Factor-alpha/metabolismABSTRACT
AIM: There have been very few paediatric studies on omentin-1, an anti-inflammatory adipokine that provides a link between adiposity, insulin resistance and metabolic syndrome. This Chinese study evaluated the association between omentin-1 and metabolic syndrome and analysed the effect of a six-month lifestyle intervention on the levels in obese children. METHODS: We recruited 119 obese outpatients (75% boys) aged 7-18 years from the Second Affiliated Hospital of Xi'an Jiaotong University, who underwent a six- month lifestyle intervention. Our controls were 55 matched children with normal weight. Anthropometric parameters, biochemical data and circulating omentin-1 levels were measured at baseline and after six months. RESULTS: Of the 119 obese children, 32 (27%) had metabolic syndrome. The obese children, particularly those with metabolic syndrome, had significantly lower serum omentin-1 levels at baseline than the controls. We also found that the omentin-1 levels were negatively associated with their body mass index, waist circumference and homoeostasis model assessment of insulin resistance. After the six-month lifestyle intervention, the obese children showed significant weight loss and their omentin-1 levels increased. CONCLUSION: Serum omentin-1 was regulated by weight and seemed to be associated with children's metabolic disorders. A six-month lifestyle intervention significantly increased serum omentin-1 levels.
