| Popis: |
Introduction: Matrix metalloproteinase-9 (MMP9) plays a key role in blood–spinal cord barrier dysfunction. MMP9 blockade leads to improved injured locomotor recovery. However, it is still unknown whether MMP9 deficiency affects gene expression or signal transduction pathways in the spinal neuron. Material and Methods: In this study, we first screen the MMP9 knockdown mice with high superoxide dismutase (SOD) expression and low MMP9 expression by polymerase chain reaction analysis. Then, the gene microarrays were used to screen differentially expressed genes in the spinal neuron from MMP-9 knockout and wild-type mice. There were six groups in this experiment, including three negative control groups: SOD_1, SOD_2, and SOD_3, and three experiment groups: SOD_ MMP9_1, SOD_ MMP9_2, and SOD_ MMP9_3. The gene ontology terms were used to predict the potential functions of these differentially expressed genes, and the Kyoto Encyclopedia of Genes and Genomes was used to analyze the potential functions of these target genes in the pathways. Results: We found that the gene expression in the spinal neuron from MMP9 knockout mice was significantly altered compared to wild-type mice. FoxO signaling, axon guidance, ubiquitin-mediated proteolysis, regulation of actin cytoskeleton, and proteoglycans were changed. Discussion and Conclusion: In summary, MMP9 plays a role in spinal neuron signaling and the underlying mechanism may through affecting several signaling pathways. |
