The molecular mechanism of premature brain injury induced by inflammation is not fully understood. Long noncoding RNAs (lncRNAs) have been reported to play crucial roles in neurological disorders including brain injury. However, little is known about the regulatory function of lncRNAs in the premature brain. This study investigates differentially expressed lncRNAs and mRNAs as well as their interactions in the premature brain. Lipopolysaccharides (LPS) were used to induce inflammation in premature rodent models. Brain histology was observed via hematoxylin and eosin (HE) staining and CD68 immunostaining. Arraystar microarry was designed for the profiling of differentially expressed lncRNAs and mRNAs in 4 LPS induced premature brains (L group), 4 full-term control brains (C group) and 3 premature brains were not induced by LPS (P group). Bioinformatic analysis was applied to reveal the functions and co-expression relationship of lncRNAs and mRNAs. Three lncRNAs and 2 mRNAs were selected for validation applying quantitative real time polymerase chain reaction (qRT-PCR). This study demonstrates dysregulated lncRNA and mRNA profiles in the premature brains upon inflammatory insult, thus revealing a novel mechanism of premature brain development from a new perspective of the lncRNAs and mRNA coexpression network and providing important insights into the therapy of premature brain injury.
Keywords: Brain injury; Inflammation; Long noncoding RNA; Preterm birth.
Copyright © 2019. Published by Elsevier B.V.