Hengxing Zhou1, Yi Kang1, Zhongju Shi1, Lu Lu1, Xueying Li2, Tianci Chu3, Jun Liu4, Lu Liu1, Yongfu Lou1, Chi Zhang1, Guangzhi Ning1, Shiqing Feng5, Xiaohong Kong6. 1. Department of Orthopaedics, Tianjin Medical University General Hospital, No. 154 Anshan Road, Heping District, Tianjin 300052, PR China; Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, No. 154 Anshan Road, Heping District, Tianjin 300052, PR China. 2. Key Laboratory of Immuno Microenvironment and Disease of the Educational Ministry of China, Department of Immunology, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, PR China. 3. Kosair Children's Hospital Research Institute at the Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA. 4. First Affiliated Hospital of Gannan Medical University, No. 23 Qingnian Road, Ganzhou 341000, PR China. 5. Department of Orthopaedics, Tianjin Medical University General Hospital, No. 154 Anshan Road, Heping District, Tianjin 300052, PR China; Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, No. 154 Anshan Road, Heping District, Tianjin 300052, PR China. Electronic address: sqfeng@tmu.edu.cn. 6. School of Medicine, Nankai University, No. 94 Weijin Road, Nankai District, Tianjin 300071, PR China. Electronic address: kongxh@nankai.edu.cn.
Abstract
BACKGROUND: Spinal cord injury (SCI) is a disease associated with high disability and mortality rates. The transitional phase from subacute phase to intermediate phase may play a major role in the process of secondary injury. Changes in protein expression levels have been shown to play key roles in many central nervous system (CNS) diseases. Nevertheless, the roles of proteins in the transitional phase of SCI are not clear. METHODS: We examined protein expression in a rat model 2 weeks after SCI and identified differentially expressed proteins (DEPs) using isobaric tagging for relative and absolute protein quantification (iTRAQ). Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of DEPs were performed. Furthermore, we constructed a protein-protein interaction (PPI) network, and the top 10 high-degree core nodes were identified. Meanwhile, we validated protein level changes of five high-degree core regulated proteins using Western blots. RESULTS: A total of 162 DEPs were identified between the injury group and the control, of which 101 (62.35%) were up-regulated and 61 (37.65%) were down-regulated in the transitional phase of SCI. Key molecular function, cellular components, biological process terms and pathways were identified and may be important mechanisms in the transitional phase of SCI. Alb, Calm1, Vim, Apoe, Syp, P4hb, Cd68, Eef1a2, Rab3a and Lgals3 were the top 10 high-degree core nodes. Western blot analysis performed on five of these proteins showed the same trend as iTRAQ results. CONCLUSION: The current study may provide novel insights into how proteins regulate the pathogenesis of the transitional phase after SCI.
BACKGROUND:Spinal cord injury (SCI) is a disease associated with high disability and mortality rates. The transitional phase from subacute phase to intermediate phase may play a major role in the process of secondary injury. Changes in protein expression levels have been shown to play key roles in many central nervous system (CNS) diseases. Nevertheless, the roles of proteins in the transitional phase of SCI are not clear. METHODS: We examined protein expression in a rat model 2 weeks after SCI and identified differentially expressed proteins (DEPs) using isobaric tagging for relative and absolute protein quantification (iTRAQ). Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of DEPs were performed. Furthermore, we constructed a protein-protein interaction (PPI) network, and the top 10 high-degree core nodes were identified. Meanwhile, we validated protein level changes of five high-degree core regulated proteins using Western blots. RESULTS: A total of 162 DEPs were identified between the injury group and the control, of which 101 (62.35%) were up-regulated and 61 (37.65%) were down-regulated in the transitional phase of SCI. Key molecular function, cellular components, biological process terms and pathways were identified and may be important mechanisms in the transitional phase of SCI. Alb, Calm1, Vim, Apoe, Syp, P4hb, Cd68, Eef1a2, Rab3a and Lgals3 were the top 10 high-degree core nodes. Western blot analysis performed on five of these proteins showed the same trend as iTRAQ results. CONCLUSION: The current study may provide novel insights into how proteins regulate the pathogenesis of the transitional phase after SCI.