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在Serratia的入侵中,E-Cadherin的宿主细胞依赖性作用
Olga Tsaplina1, Ekaterina Lomert1, Yuliya Berson1
1Institute of Cytology, Russian Academy of Sciences, Tikhoretsky av. 4, 194064 St Petersburg, Russia.
International journal of molecular sciences
|December 9, 2023
概括
塞拉提亚蛋白质虫的入侵仅依赖于全长的E-cadherin,而塞拉提亚灰色虫的入侵则使用全长和截断的E-cadherin. 在S. grimesii的入侵中,截断的E-cadherin形成与积累和蛋白酶活性有关.
科学领域:
- 微生物学和细胞生物学
- 宿主-病原体相互作用
- 细菌入侵的分子机制
背景情况:
- 细菌利用细胞表面蛋白质进行宿主-病原体相互作用和宿主细胞进入.
- 细胞粘附蛋白质E-cadherin作为细菌进入的受体.
- 以前的研究将对Serratia grimesii的真核细胞敏感性增加与E-cadherin表达的增加联系起来.
研究的目的:
- 调查E-cadherin在M-HeLa和Caco-2细胞被Serratia grimesii和Serratia proteamaculans入侵中的作用.
- 在细菌入侵中区分全长与截断的E-cadherin的参与.
- 阐明参与E-cadherin介导细菌进入的信号通路和宿主因素.
主要方法:
- 细菌感染后M-HeLa和Caco-2细胞中E-cadherin表达的量化.
- 使用分子技术在感染细胞中分析E-cadherin形式 (全长或截断).
- 使用siRNA向E-cadherin和药理抑制剂 (ADAM10,EGFR) 的抑制研究,以评估它们对细菌入侵的影响.
主要成果:
- 细菌感染在两个细胞系中增加了E-cadherin的表达.
- 仅在Caco-2细胞中,Serratia proteamaculans的入侵被E-cadherin siRNA抑制,这表明它依赖于全长的E-cadherin.
- 在两种细胞系中,E-cadherin siRNA抑制了Serratia grimesii的入侵,这表明包括全长和截断的E-cadherin. 截断的E-cadherin形成和随后的EGFR信号与积和ADAM10活性有关.
结论:
- 全长的E-cadherin对于Serratia proteamaculans入侵是必不可少的.
- 全长和截断的E-cadherin都对Serratia grimesii的入侵有所贡献.
- 通过细菌蛋白酶或ADAM10激活 (与流入相关) 生成的截断的E-cadherin,在Serratia grimesii进入和EGFR信号传递中发挥作用.
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