作者: Jia‐He Chen , Dan‐Dan Feng , Yu‐Fei Chen , Cai‐Xia Yang , Chen‐Xia Juan
DOI: 10.1111/JCMM.15661
关键词:
摘要: Bronchopulmonary dysplasia (BPD) is a severe complication of preterm infants characterized by increased alveolarization and inflammation. Premature exposure to hyperoxia believed be key contributor the pathogenesis BPD. No effective preventive or therapeutic agents have been created. Stimulator interferon gene (STING) associated with inflammation apoptosis in various lung diseases. Long non-coding RNA MALAT1 has reported involved However, how regulates STING expression remains unknown. In this study, we assessed that were up-regulated tissue from BPD neonates, hyperoxia-based rat models epithelial cell lines. Then, using flow cytometry proliferation assay, found down-regulating inhibited promoted hyperoxia-treated cells. Subsequently, qRT-PCR, Western blotting dual-luciferase reporter assays showed suppressing decreased promoter activity STING. Moreover, transcription factor CREB its regulatory role via chromatin immunoprecipitation. conclusion, interacts regulate neonates. STING, may promising targets prevention treatment