在SARS-CoV-2中,S蛋白的表达驱动了内皮细胞中的合成细胞的形成
Katie V Tieu1, Madaline Espey2, Aarthi Narayanan3,4
1Department of Biomedical Engineering, The Ohio State University, Columbus, OH, USA.
Scientific reports
|January 28, 2025
概括
SARS-CoV-2 感染导致上皮细胞形成 syncytia. 这项研究表明,SARS-CoV-2 S蛋白还会诱导内皮细胞中的合成细胞,影响心血管健康.
科学领域:
- 细胞生物学 细胞生物学
- 病毒学 病毒学
- 心血管科学 心血管科学
背景情况:
- SARS-CoV-2 感染主要影响上皮细胞,导致结合细胞的形成.
- COVID-19经常出现心血管症状,这表明更广泛的细胞点.
- 内皮细胞形成血管的内壁,在心血管健康中起着关键作用.
研究的目的:
- 为了调查SARS-CoV-2的S蛋白表达是否会诱导内皮细胞中合成细胞的形成.
- 探索在内皮细胞中S蛋白诱导的突触中涉及的机制和细胞因素.
- 为了确定内皮细胞是否易受SARS-CoV-2感染并导致COVID-19病理.
主要方法:
- 在内皮细胞中表达的SARS-CoV-2 S蛋白和评估的突触形成.
- 研究了髓轻链激酶 (MLCK) 和Rho相关蛋白激酶 (ROCK) 的作用.
- 评估了不同硬度的基板上和机械应力下 (双轴拉伸,剪切应力) 的结合膜形成.
- 感染了SARS-CoV-2的内皮细胞,以确认易感性并观察结合细胞的形成.
主要成果:
- 内皮细胞中的S蛋白表达诱导了合成细胞的形成,大约10%的细胞形成了含有平均6个核的合成细胞.
- 合成细胞形成与细胞之间的间隙有关,可能会损害屏障功能.
- 抑制MLCK和降低基质刚度降低了合成细胞的形成,这表明细胞收缩性发挥了作用.
- 流体剪切应力减少了突触形成,而双轴拉伸没有影响.
- 内皮细胞支持SARS-CoV-2感染和复制,病毒感染也会诱导合成细胞.
结论:
- 内皮细胞是SARS-CoV-2感染的易受宿主.
- 在内皮细胞中SARS-CoV-2的S蛋白表达会导致结合细胞的形成,这可能会导致COVID-19中的心血管病理.
- 细胞收缩性受到MLCK和基质刚性的影响,在合成细胞形成中起作用.
- 像流体剪切应力这样的机械力量可以调节内皮细胞中的合成细胞的形成.
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