MicroRNA-590-5p represses proliferation of human fetal airway smooth muscle cells by targeting signal transducer and activator of transcription 3

Introduction: Pediatric asthma has remained a health threat to children in recent years. The abnormal proliferation of airway smooth muscle (ASM) cells contributes to airway remodeling during development of asthma. Mi-croRNAs (miRNAs) are critical regulators of ASM cell proliferation during airway remodeling. miR-590-5p has been reported to regulate cell prolifera-tion in various cell types. However, it remains unclear whether miR-590-5p regulates ASM cell proliferation. In this study, we aimed to investigate the potential role of miR-590-5p in regulating fetal ASM cell proliferation in vitro stimulated by platelet-derived growth factor (PDGF). Material and methods: miRNA, mRNA, and protein expression was detected by real-time quantitative polymerase chain reaction and western blot. Cell proliferation was detected by CCK-8 and BrdU assays. The target of miR-590-5p was confirmed by dual-luciferase reporter assay. Results: MiR-590-5p expression was significantly down-regulated in fetal ASM cells stimulated with PDGF (p < 0.05). Overexpression of miR-590-5p inhibited cell proliferation (p < 0.05), whereas the suppression of miR-590-5p promoted cell proliferation of fetal ASM cells stimulated with PDGF (p < 0.05). Signal transducer and activator of transcription 3 (STAT3) was identified as a target gene of miR-590-5p. In addition, miR-590-5p negatively regulated STAT3 expression (p < 0.05). Moreover, miR-590-5p also modulated downstream genes of STAT3 including cyclin D3 and p27 (p < 0.05). The res-toration of STAT3 significantly reversed the inhibitory effect of miR-590-5p on fetal ASM cell proliferation. Conclusions: MiR-590-5p inhibits proliferation of fetal ASM cells by down-regulating STAT3, thereby suggesting a novel therapeutic target for the treatment of pediatric asthma.