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基于生物信息学分析鉴定脊髓损伤的关键基因和通路。

Identification of pivotal genes and pathways for spinal cord injury via bioinformatics analysis.

机构信息

Department of Orthopedics, Shanghai Tian You Hospital, Shanghai 200331, P.R. China.

Department of Orthopedics, Shanghai General Hospital, Shanghai 200080, P.R. China.

出版信息

Mol Med Rep. 2017 Oct;16(4):3929-3937. doi: 10.3892/mmr.2017.7060. Epub 2017 Jul 21.

DOI:10.3892/mmr.2017.7060
PMID:28731189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5646972/
Abstract

The present study aimed to identify key genes and pathways associated with spinal cord injury (SCI) and subsequently investigate possible therapeutic targets for the condition. The array data of GSE20907 was downloaded from the Gene Expression Omnibus database and 24 gene chips, including 3‑day, 4‑day, 1‑week, 2‑week and 1‑month post‑SCI together with control propriospinal neurons, were used for the analysis. The raw data was normalized and then the differentially expressed genes (DEGs) in the (A) 2‑week post‑SCI group vs. control group, (B) 1‑month post‑SCI group vs. control group, (C) 1‑month and 2‑week post‑SCI group vs. control group, and (D) all post‑SCI groups vs. all control groups, were analyzed with a limma package. Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses for DEGs were performed. Cluster analysis was performed using ClusterOne plugins. All the DEGs identified were associated with immune and inflammatory responses. Signal transducer and activator of transcription 3 (STAT3), erb‑B2 receptor tyrosine kinase 4 (ERBB4) and cytochrome B‑245, α polypeptide (CYBA) were in the network diagrams of (A), (C) and (D), respectively. The enrichment analysis of DEGs identified in all samples demonstrated that the DEGs were also enriched in the chemokine signaling pathway (enriched in STAT3) and the high‑affinity immunoglobulin E receptor (FcεRI) signaling pathway [enriched in proto‑oncogene, src family tyrosine kinase (LYN)]. Immune and inflammatory responses serve significant roles in SCI. STAT3, ERBB4 and CYBA may be key genes associated with SCI at certain stages. Furthermore, STAT3 and LYN may be involved in the development of SCI via the chemokine and FcεRI signaling pathways, respectively.

摘要

本研究旨在鉴定与脊髓损伤(SCI)相关的关键基因和途径,并随后研究该疾病的可能治疗靶点。从基因表达综合数据库中下载 GSE20907 的阵列数据,使用包括 3 天、4 天、1 周、2 周和 1 个月 SCI 后以及对照 propriospinal 神经元的 24 个基因芯片进行分析。对原始数据进行标准化,然后使用 limma 包分析(A)2 周 SCI 后组与对照组、(B)1 个月 SCI 后组与对照组、(C)1 个月和 2 周 SCI 后组与对照组、(D)所有 SCI 后组与所有对照组之间的差异表达基因(DEGs)。对 DEGs 进行基因本体注释和京都基因与基因组百科全书通路富集分析。使用 ClusterOne 插件进行聚类分析。鉴定的所有 DEGs 均与免疫和炎症反应有关。信号转导和转录激活因子 3(STAT3)、表皮生长因子受体酪氨酸激酶 4(ERBB4)和细胞色素 B-245,α 多肽(CYBA)分别位于(A)、(C)和(D)的网络图中。所有样本中鉴定的 DEGs 的富集分析表明,DEGs 还富集于趋化因子信号通路(在 STAT3 中富集)和高亲和力免疫球蛋白 E 受体(FcεRI)信号通路[在原癌基因,src 家族酪氨酸激酶(LYN)中富集]。免疫和炎症反应在 SCI 中起着重要作用。STAT3、ERBB4 和 CYBA 可能是与特定阶段 SCI 相关的关键基因。此外,STAT3 和 LYN 可能分别通过趋化因子和 FcεRI 信号通路参与 SCI 的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/dcd1cedb2564/MMR-16-04-3929-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/64fbefa01d99/MMR-16-04-3929-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/76c948d997d5/MMR-16-04-3929-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/f71d59c5d448/MMR-16-04-3929-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/919f37296de8/MMR-16-04-3929-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/9857af73ba42/MMR-16-04-3929-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/119c0a11792a/MMR-16-04-3929-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/215e301f64bd/MMR-16-04-3929-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/dcd1cedb2564/MMR-16-04-3929-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/64fbefa01d99/MMR-16-04-3929-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/76c948d997d5/MMR-16-04-3929-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/f71d59c5d448/MMR-16-04-3929-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/919f37296de8/MMR-16-04-3929-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/9857af73ba42/MMR-16-04-3929-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/119c0a11792a/MMR-16-04-3929-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/215e301f64bd/MMR-16-04-3929-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7edf/5646972/dcd1cedb2564/MMR-16-04-3929-g07.jpg

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