MicroRNA‑204 may participate in the pathogenesis of hypoxic‑ischemic encephalopathy through targeting KLLN

摘要: Hypoxic-ischemic encephalopathy (HIE) is a common neonatal disease that can lead to high mortality rates. Previous studies have indicated microRNAs (miRs) may be involved in the pathogenesis of HIE; however, specific mechanisms underlying their involvement require further investigation. The aim present study was investigate roles miR-204 and its target gene killin p53 regulated DNA replication inhibitor (KLLN) HIE using rat models. Brain injury induced by surgery incubation hypoxic incubator brain 10-day-old pup rats. On day 3, rats were sacrificed, infarct size determined tetrazolium chloride assay. Terminal deoxynucleotidyl transferase UTP nick-end labeling staining performed detect cell death rate tissue. Following this, tissues collected, reverse transcription-quantitative polymerase chain reaction, western blot analysis immunohistochemistry assays examine expression levels KLLN. Furthermore, neurons cultured transfected with inhibitors or mimics, effect on proliferation apoptosis examined MTT flow cytometric assays. Finally, dual-luciferase reporter assay confirm whether KLLN direct miR-204. significantly downregulated increased tissue (P<0.001). In addition, transfection decreased rates neurons; mimics prompted opposite results. also confirmed Taken together, results demonstrated serve important through targeting