慢性静力性损伤模型家兔颈后肌群转录组学的生物信息分析

关键词：慢性静力性损伤  颈肌损伤  转录组测序  差异表达基因

Keywords:chronic static injury  cervical muscle injuries  transcriptome sequencing  differentially expressed genes

摘要：

      摘要 目的：利用转录组测序分析技术研究慢性静力性损伤模型家兔颈后肌的差异表达基因（DEGs）和关键信号通路。 方法：通过长期反复屈曲家兔颈部复制兔颈后肌慢性静力负荷损伤模型。利用转录组测序技术筛选DEGs并进行 GO功能富集和KEGG通路富集分析。构建PPI网络，筛选出前10位的DEGs。 结果：与空白组相比，共有310个DEGs，其中上调193个，下调117个；GO分析显示，模型组差异基因主要涉及炎症和免疫反应调节等相关功能；KEGG分析显示吞噬体与Fcγ-R介导的吞噬作用、NF-κB等信号通路表现活跃。PPI网络确定了10个hub基因，其中TLR4、CTSS、ITGB2、TYROBP、CD74、LAPTM5等表达上调，仅PPARG表达下调。 结论：颈肌慢性静力性损伤的病理变化涉及众多基本的生物学过程，炎症反应及免疫微环境的紊乱在其中发挥着重要作用；与炎症反应密切相关的差异基因以及NF-κB信号通路、吞噬体、Fcγ-R 介导的吞噬作用等通路分子的转录激活可能是其主要的分子机制。

Abstract:

      Abstract Objective： Transcriptome sequencing analysis was used to study the differentially expressed genes （DEGs） and key signaling pathways of the posterior cervical muscles of rabbits in a model of chronic static injury. Method： The chronic static load injury model of posterior cervical muscle in rabbits was replicated by long-term repeated flexion of the neck of rabbits. DEGs were screened by transcriptome sequencing and analyzed for GO function enrichment and KEGG pathway enrichment. Build a PPI network and filter out the top 10 DEGs. Result： Compared with the blank group， there were 310 DEGs， of which 193 were upward and 117 were downward in the model group. GO analysis showed that the different genes in the model group were mainly involved in related functions such as inflammation and immune response regulation. KEGG analysis showed that phagosomes were active in Fcγ-R-mediated phagocytosis and NF-κB. The PPI network identified 10 hub genes， among which TLR4， CTSS， ITGB2， TYROBP， CD74， LAPTM5 and other expressions were up-regulated， and only PPARG expression was down-regulated. Conclusion： The pathological changes of chronic static injury of cervical muscles involve plenty of basic biological processes， and the inflammatory response and the disorder of immune microenvironment play an important role in it. Transcriptional activation of differential genes closely related to inflammatory responses and pathway molecules such as NF-κB signaling pathway， phagosomes， and Fcγ-R-mediated phagocytosis may be its main molecular mechanisms.