Abstract
Long noncoding RNAs (LncRNAs) play a crucial role in cell growth, development, and various diseases related to the central nervous system. However, LncRNA differential expression profiles in spinal cord injury are yet to be reported. In this study, we profiled the expression pattern of LncRNAs using a microarray method in a contusion spinal cord injury (SCI) mouse model. Compared with a spinal cord without injury, few changes in LncRNA expression levels were noted 1 day after injury. The differential changes in LncRNA expression peaked 1 week after SCI and subsequently declined until 3 weeks after injury. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to validate the reliability of the microarray, demonstrating that the results were reliable. Gene ontology (GO) analysis indicated that differentially expressed mRNAs were involved in transport, cell adhesion, ion transport, and metabolic processes, among others. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that the neuroactive ligand-receptor interaction, the PI3K-Akt signaling pathway, and focal adhesions were potentially implicated in SCI pathology. We constructed a dynamic LncRNA-mRNA network containing 264 LncRNAs and 949 mRNAs to elucidate the interactions between the LncRNAs and mRNAs. Overall, the results from this study indicate for the first time that LncRNAs are differentially expressed in a contusion SCI mouse model.
Highlights
Spinal cord injury (SCI) has become a global burden, influencing the quality of life and triggering serious socioeconomic consequences
Our research provides the first evidence of an aberrant Long noncoding RNAs (LncRNAs) expression profile in SCI
The microarray data (Table 2) indicated that the LncRNA and mRNA expression dynamically changed from the initial injury to 1 day, 3 days, 1 week, and 3 weeks after injury
Summary
Spinal cord injury (SCI) has become a global burden, influencing the quality of life and triggering serious socioeconomic consequences. Having SCI means being confined to a wheelchair and a lifetime of medical disease [1]. Repairing SCI is challenging due to multiple factors, including extensive cell loss, axonal disruption, growth-inhibiting molecules in the scar, and a lack of growth-promoting molecules [2]. Several studies have indicated that changes in various cellular events are significantly associated with SCI. Among these changes is the dysregulated gene expression of specific molecules. Abnormal gene expression is a highly complex process
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