[生物信息学分析和毒症关键基因验证基于GEO数据库的心肌巨微阵列数据]
1Department of Rehabilitation, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Zhonghua xin xue guan bing za zhi
|July 17, 2023
概括
生物信息学确定了细胞因子信号传递3 (Socs3) 抑制剂,干白素1受体对抗剂 (Il1rn) 和化学因子C-C动机配体7 (Ccl7) 作为败血症诱导心肌损伤的关键基因. 这些基因在心脏巨细胞中被上调,并显示出作为诊断和治疗点的潜力.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 生物信息学是一种生物信息学.
背景情况:
- 败血症引起的心肌损伤是败血症的一个关键并发症.
- 确定涉及败血症引起的心肌损伤的分子机制和关键基因对于开发有效治疗非常重要.
研究的目的:
- 通过生物信息学分析,在败血症诱导的心肌损伤期间,在心脏巨中识别差异表达基因 (DEGs).
- 在体内和体外验证参与败血症诱导心肌损伤的病原发生的关键基因.
主要方法:
- 基因芯片数据 (GSE104342) 分析,以确定败血性小鼠心脏巨细胞中的DEGs.
- 基因本体学和KEGG通路丰富分析,以了解DEGs的功能.
- 使用STRING和Cytoscape进行蛋白质与蛋白质相互作用网络分析,以确定枢纽基因.
- 用于验证,构建了败血症和RAW264.7巨细胞体外培养的小鼠模型.
主要成果:
- 确定了177个DEG,主要涉及炎症和免疫反应.
- 关键基因 细胞因子信号传递3 (Socs3) 的抑制剂,介素1受体对手 (Il1rn) 和化学因子C-C动机连接体7 (Ccl7) 被确定为枢纽基因.
- 在体内研究表明心脏功能下降,心肌细胞亡增加,在败血症小鼠中Socs3,Il1rn和Ccl7的上调调节.
- 在体外研究证实了 Socs3,Il1rn 和 Ccl7 在用脂多糖 (LPS) 刺激的巨细胞中的上调.
结论:
- Socs3,Il1rn和Ccl7在败血症引起的心肌损伤期间在心肌巨中显著上调.
- 这些关键基因是潜在的诊断标记物和毒引起的心脏损伤的治疗点.
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