Repair mechanism of astrocytes and non-astrocytes in spinal cord injury

Xiang-Yun Liu; Jian-Wei Guo; Jian-Qiang Kou; Yuan-Liang Sun; Xiu-Jun Zheng

doi:10.12998/wjcc.v8.i5.854

Repair mechanism of astrocytes and non-astrocytes in spinal cord injury

World J Clin Cases. 2020 Mar 6;8(5):854-863. doi: 10.12998/wjcc.v8.i5.854.

Authors

Xiang-Yun Liu¹, Jian-Wei Guo¹, Jian-Qiang Kou¹, Yuan-Liang Sun¹, Xiu-Jun Zheng²

Affiliations

¹ Department of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong Province, China.
² Department of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong Province, China. xiyi5148141@163.com.

Abstract

Background: Spinal cord injury (SCI) is a destructive disease that incurs huge personal and social costs, and there is no effective treatment. Although the pathogenesis and treatment mechanism of SCI has always been a strong scientific focus, the pathogenesis of SCI is still under investigation.

Aim: To determine the key genes based on the modularization of in-depth analysis, in order to identify the repair mechanism of astrocytes and non-astrocytes in SCI.

Methods: Firstly, the differences between injured and non-injured spinal cord of astrocyte (HA), injured and non-injured spinal cord of non-astrocyte (FLOW), injured spinal cord of non-injured astrocyte (HA) and non-injured spinal cord of non-astrocyte (FLOW), and non-injured spinal cord of astrocyte (HA) and non-astrocyte (FLOW) were analyzed. The total number of differentially expressed genes was obtained by merging the four groups of differential results. Secondly, the genes were co-expressed and clustered. Then, the enrichment of GO function and KEGG pathway of module genes was analyzed. Finally, non-coding RNA, transcription factors and drugs that regulate module genes were predicted using hypergeometric tests.

Results: In summary, we obtained 19 expression modules involving 5216 differentially expressed genes. Among them, miR-494, XIST and other genes were differentially expressed in SCI patients, and played an active regulatory role in dysfunction module, and these genes were recognized as the driving genes of SCI. Enrichment results showed that module genes were significantly involved in the biological processes of inflammation, oxidation and apoptosis. Signal pathways such as NF-kappa B/A20, AMPK and MAPK were significantly regulated. In addition, non-coding RNA pivot (including miR-136-5p and let-7d-5p, etc.) and transcription factor pivot (including NFKB1, MYC, etc.) were identified as significant regulatory dysfunction modules.

Conclusion: Overall, this study uncovered a co-expression network of key genes involved in astrocyte and non-astrocyte regulation in SCI. These findings helped to reveal the core dysfunction modules, potential regulatory factors and driving genes of the disease, and to improve our understanding of its pathogenesis.

Keywords: Astrocyte; Dysfunction module; Module genes; Non-astrocyte; Repair mechanism; Spinal cord injury.