microrna-29a-3p accelerates inflammatory damage in neonatal pneumonia via targeting krüppel-like factor 4

Neonatal pneumonia (np) is a frequently occurring illness during the neonatal phase. the study investigated the molecular process and the role of microrna (mir)-29a-3p in np.peripheral blood was collected from np patients and healthy newborns. human lung fibroblasts cell line (wi-38) were treated with lipopolysaccharide (lps)) to establish a cellular model for np. then, mir-29a-3p and krüppel-like factor 4 (klf4) levels were detected by rt-qpcr or western blot. the relationship between mir-29a-3p and klf4 was confirmed by dual luciferase reporter gene assay. cell survival was assessed using the cck-8 assay, whereas the levels of interleukin-6, tumor necrosis factor-α, and il-1β were quantified using elisa. additionally, apoptosis was evaluated through flow cytometry. meanwhile, bax and bcl-2 were detected by rt-qpcr. neonatal rats were administered lps intraperitoneally (3 mg/kg) to induce np, and pathological injury and inflammatory reaction were analyzed.mir-29a-3p was elevated but klf4 was silenced in np patient’s serum, lps-treated wi-38 cell line, and lps-treated newborn rats. silence of mir-29a-3p or elevation of klf4 constrained cell proliferation with inflammation of lps-treated wi-38 cell line. mir-29a-3p immediately targeted klf4. additionally, silence of mir-29a-3p alleviated lps-stimulated lung injury and inflammation in neonatal rats. the protective action of silenced mir-29a-3p in lps-treated wi-38 cell line and newborn rats was turned around by silencing klf4.this study demonstrates originally that mir-29a-3p boosts inflammatory damage in np via targeting klf4, offering a basis for clinically diagnosing and treating np.