Profiling analysis reveals the potential contribution of long non-coding RNAs to preterm white matter injury.

Abstract Aims The aim of this study was to investigate the molecular mechanism underlying preterm white matter injury (WMI) via the identification and functional analysis of differentially expressed long non-coding RNAs (lncRNAs) and mRNAs. Main methods A neonatal rat model of preterm WMI was established by ligating the common carotid artery and hypoxia induction. RNA sequencing was performed to analyze gene expression profiles of brain samples. Gene Ontology (GO) and Kyoto Encyclopedia of Genes (KEGG) analyses were performed to evaluate functions of target mRNAs. A co-expression network was generated to explore regulatory mechanisms. Key findings In total, 210 lncRNAs and 619 mRNAs were differentially expressed between the preterm WMI group and the control group. Based on GO and KEGG analyses, enriched pathways included the apoptotic signaling pathway, vascular endothelial growth factor (VEGF) signaling pathway, natural killer cell-mediated cytotoxicity pathway, and the autophagy pathway. Significance Differentially expressed lncRNAs and mRNAs in the brain tissues of preterm WMI model were identified, and the biological processes were closely associated with the development of preterm WMI, thus being considered potential targets for future studies.