Molecular Expression Profile of Changes in Rat Acute Spinal Cord Injury.

Molecular Expression Profile of Changes in Rat Acute Spinal Cord Injury.
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DOI:
10.3389/fncel.2021.720271
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发表时间:
2021
影响因子:
5.3
通讯作者:
Zhou J
Zhou J
中科院分区:
医学2区
文献类型:
--
作者:
Wang JJ;Ye G;Ren H;An CR;Huang L;Chen H;Zhang H;Lin JX;Shen X;Heng BC;Zhou J

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背景:脊髓损伤(SCI)是一种具有多种病因的高致死率和致残性疾病。到目前为止,还没有有效的治疗方法可以完全治愈。脊髓损伤在分子、基因和蛋白表达水平上的病理机制尚不清楚。方法:本研究采用单细胞转录组学分析和蛋白芯片分析,分别分析大鼠脊髓损伤部位周围细胞基因表达谱和炎症因子分泌的变化。结果:单细胞转录组学分析发现,三种类型的胶质细胞(小胶质细胞、星形胶质细胞和少突胶质细胞)在急性损伤后被激活,氧化石墨烯在损伤后表现出多种炎症相关的特性,如代谢过程、免疫调节和抗原呈递。蛋白芯片结果显示,损伤后4种有利于损伤修复的炎性细胞因子水平降低,9种阻碍损伤修复的炎性细胞因子水平升高。结论:这些发现揭示了脊髓损伤后细胞状态从稳态到反应性的变化,有助于了解脊髓损伤后的病理过程,以及神经胶质细胞与炎症因子之间的潜在关系,为进一步阐明继发性脊髓损伤的分子机制提供了新的理论基础。
Background: Spinal cord injury (SCI) is a highly lethal and debilitating disease with a variety of etiologies. To date, there is no effective therapeutic modality for a complete cure. The pathological mechanisms of spinal cord injury at the molecular gene and protein expression levels remain unclear. Methods: This study used single-cell transcriptomic analysis and protein microarray analysis to analyzes changes in the gene expression profiles of cells and secretion of inflammatory factors respectively, around the lesion site in a rat SCI model. Results: Single-cell transcriptomic analysis found that three types of glial cells (microglia, astrocyte, and oligodendrocyte) becomes activated after acute injury, with GO exhibiting a variety of inflammatory-related terms after injury, such as metabolic processes, immune regulation, and antigen presentation. Protein microarray results showed that the levels of four inflammatory cytokines favoring SCI repair decreased while the levels of nine inflammatory cytokines hindering SCI repair increased after injury. Conclusion: These findings thus reveal the changes in cellular state from homeostatic to reactive cell type after SCI, which contribute to understand the pathology process of SCI, and the potential relationship between glial cells and inflammatory factors after SCI, and provides new theoretical foundation for further elucidating the molecular mechanisms of secondary SCI.
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