Zhang Yue-Hui, Song Jia, Wang Li-Gang, Shao Jiang
Department of Orthopedic Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.
Mol Med Rep. 2017 Apr;15(4):1577-1584. doi: 10.3892/mmr.2017.6192. Epub 2017 Feb 10.
The present study was designed to identify key genes or significant signaling pathways associated with spinal cord injury (SCI), and to clarify the underlying molecular mechanisms of SCI. Data from the GSE45550 array were downloaded from the Gene Expression Omnibus database. A total of 6 control samples, 6 samples at 3 days post‑SCI (SCI3d), 6 samples at 8 days post‑SCI (SCI8d) and 6 samples at 14 days post‑SCI (SCI14d) were included. The microarray data was preprocessed by the robust multi‑array average algorithm. The differentially expressed genes (DEGs) were identified using the limma package. The overlapping DEGs among groups were analyzed using the Venny 2.0 online tool. Modules enriched by DEGs were selected by weighted gene co‑expression network analysis. Gene Ontology annotation and the Kyoto Encyclopedia of Genes and Genomes pathways were identified for DEGs using the Database for Annotation, Visualization and Integrated Discovery. A total of 693 genes were obtained by combining the DEGs of the SCI3d, SCI8d and SCI14d groups. The pink module and green module with smaller P‑values obtained from weighted gene co‑expression network analysis module analyses of DEGs demonstrated a higher correlation with SCI. In addition, the peroxisome proliferator‑activated receptor (PPAR) signaling pathway that the cluster of differentiation 36 (CD36) was significantly enriched in, was one of the significant pathways in the pink module. The p53 signaling pathway that Caspase‑3 (Casp3) was significantly enriched in was one of the significant pathways in the green module. In conclusion, the results of the present study demonstrated that the PPAR and p53 signaling pathway may serve important roles in the progression of SCI. In addition, CD36 and Casp3 may be involved in the progression of SCI via the PPAR and p53 signaling pathways, respectively.
本研究旨在识别与脊髓损伤（SCI）相关的关键基因或重要信号通路，并阐明SCI潜在的分子机制。从基因表达综合数据库下载了GSE45550阵列的数据。总共纳入了6个对照样本、6个SCI后3天（SCI3d）的样本、6个SCI后8天（SCI8d）的样本和6个SCI后14天（SCI14d）的样本。微阵列数据通过稳健多阵列平均算法进行预处理。使用limma软件包识别差异表达基因（DEG）。使用Venny 2.0在线工具分析各组之间重叠的DEG。通过加权基因共表达网络分析选择由DEG富集的模块。使用注释、可视化和综合发现数据库对DEG进行基因本体注释和京都基因与基因组百科全书通路分析。通过合并SCI3d、SCI8d和SCI14d组的DEG共获得693个基因。从DEG的加权基因共表达网络分析模块分析中获得的P值较小的粉色模块和绿色模块与SCI具有更高的相关性。此外，分化簇36（CD36）显著富集的过氧化物酶体增殖物激活受体（PPAR）信号通路是粉色模块中的重要通路之一。Caspase-3（Casp3）显著富集的p53信号通路是绿色模块中的重要通路之一。总之，本研究结果表明，PPAR和p53信号通路可能在SCI进展中起重要作用。此外，CD36和Casp3可能分别通过PPAR和p53信号通路参与SCI的进展。
