RNA-seq 揭示 Nup62 可能是调控创伤性脑损伤后小鼠海马区细胞分裂的关键因子。

RNA-seq reveals Nup62 as a potential regulator for cell division after traumatic brain injury in mice hippocampus.

机构信息

Department of Neurosurgery, Suzhou Science & Technology Town Hospital, Suzhou, Jiangsu Province, China.

Department of Neurosurgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, Shanghai, China.

出版信息

PeerJ. 2023 Mar 7;11:e14913. doi: 10.7717/peerj.14913. eCollection 2023.

DOI:10.7717/peerj.14913

PMID:36908815

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10000302/

Abstract

BACKGROUND

Hippocampus impairment is a common condition encountered in the clinical diagnosis and treatment of traumatic brain injury (TBI). Several studies have investigated this phenomenon. However, its molecular mechanism remains unclear.

METHODS

In this study, Illumina RNA-seq technology was used to determine the gene expression profile in mice hippocampus after TBI. We then conducted bioinformatics analysis to identify the altered gene expression signatures and mechanisms related to TBI-induced pathology in the hippocampus. Real-time quantitative polymerase chain reaction and western blot were adopted to verify the sequencing results.

RESULTS

The controlled cortical impact was adopted as the TBI model. Hippocampal specimens were removed for sequencing. Bioinformatics analysis identified 27 upregulated and 17 downregulated differentially expressed genes (DEGs) in post-TBI mouse models. Potential biological functions of the genes were determined Gene Set Enrichment Analysis (GSEA)-based Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, which suggested a series of functional changes in the nervous system. Specifically, the nucleoporin 62 (Nup62) DEG was discussed and verified. Gene ontology biological process enriched analysis suggests that the cell division was upregulated significantly. The present study may be helpful for the treatment of impaired hippocampus after TBI in the future.

摘要

背景

海马损伤是创伤性脑损伤（TBI）临床诊断和治疗中常见的情况。已有几项研究对此现象进行了探讨，但其中的分子机制仍不清楚。

方法

本研究采用 Illumina RNA-seq 技术，检测 TBI 后小鼠海马中的基因表达谱。然后，我们进行了生物信息学分析，以鉴定与 TBI 诱导的海马病理学相关的差异表达基因（DEG）的表达特征和机制。采用实时定量聚合酶链反应和蛋白质印迹法验证测序结果。

结果

采用皮质控制冲击法构建 TBI 模型，切除海马组织进行测序。生物信息学分析鉴定出 TBI 模型小鼠海马中 27 个上调和 17 个下调的差异表达基因（DEG）。基于基因集富集分析（GSEA）的基因本体论（GO）和京都基因与基因组百科全书（KEGG）分析确定了基因的潜在生物学功能，提示神经系统发生了一系列功能变化。具体讨论和验证了核孔蛋白 62（Nup62）的 DEG。GO 生物过程富集分析表明细胞分裂显著上调。本研究可能有助于未来 TBI 后受损海马的治疗。