MiR-181c-5p Suppresses MAPK1 Transcription During Fetal Distress and Regulates the Sensitivity of Neurons to Hypoxia-Induced Apoptosis.

Abstract

To examine the expression pattern of microRNA-181c-5p (miR-181c-5p) in fetal distress and explore its influence on neuronal apoptosis.Quantitative real-time polymerase chain reaction measurement of miR-181c-5p. Enzyme-linked immunosorbent assay was utilized for the examination of apoptosis-related proteins. A fetal distress model was established with oxygen-glucose deprivation/reoxygenation (OGD/R). Cell counting kit-8 and flow cytometry were used to evaluate cellular behaviors. Luciferase reporter assay was employed for target confirmation.MiR-181c-5p was markedly declined in rats with fetal distress. Caspase-3 was distinctly elevated, and survivin was distinctly attenuated in rat models with fetal distress. Overexpression of miR-181c-5p led to a significant promotion of cell viability and a suppression of cell apoptosis in the OGD/R cell model, the appearance of which was rescued by overexpression of mitogen-activated protein kinase 1 (MAPK1).MiR-181c-5p is likely involved in the regulation of neuronal cell growth and apoptosis associated with fetal distress.