Publication date: Available online 26 August 2017
Source:Acta Histochemica
Author(s): Zhuangchen Zhu, Defeng Wang, Wei Jiao, Guang Chen, Yan Cao, Qingfu Zhang, Junqin Wang
PurposeThis study aimed to explore the potential genes and pathways regulated in spinal cord injury (SCI) model mice with IL-1α and IL-1β knockout (KO).MethodsGene expression profile GSE70302, which includes data from injured spinal cord of 4 IL-1α-KO mice, 4 IL-1β-KO mice and 4 C57BL with 6 mice as controls was downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) of the IL-1α-KO or IL-1β-KO vs. control, and IL-1α-KO vs. IL-1β-KO groups were screened, followed by function enrichment and protein–protein interaction (PPI) analyses. Finally, miRNAs associated with SCI that may target the DEGs were predicted.ResultsA total of 579 and 992 DEGs were selected from the IL-1α-KO vs. control group and the IL-1β-KO vs. control group, respectively, and 208 genes common between the 2 comparison groups were identified. Additionally, 526 DEGs were identified from the IL-1α-KO vs. IL-1β-KO groups. These DEGs were significantly enriched in functions and pathways associated with ion transport, neuron apoptotic processes and inflammatory responses. The common genes were enriched in the pathways for cytokine–cytokine receptor interaction. DEGs of IL-1α-KO vs. IL-1β-KO were significantly enriched in the immune system, hematopoietic cell lineage and PI3K-Akt signalling pathway-associated biological processes and pathways. The PPI network consisted of 76 nodes, such as Saa2, Kcna1, Scn8a, Ccl5, Ccl28 and Pink1. A total of 94 miRNAs, including mir-17-5P and mir-30a-5p were predicted that could target the DEGs.ConclusionIL-1α and IL-1β may play important roles in SCI by regulating ion transport, inflammation and neuron apoptotic processes and their associated genes or miRNAs. Compared with IL-1β-KO, IL-1α-KO may improve the outcome of SCI via the alteration of hematopoietic cell lineage and PI3K-Akt signalling pathways.
http://ift.tt/2wg1cFl
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