ангиотензин I 和 II 刺激 SARS-CoV-2 的细胞入侵:通过抑制 RAS 的 ACE2 臂的潜在机制
S Zorad1, M Skrabanova, M Zilkova
1Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic. stefan.zorad@savba.sk and Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovak Republic. peter.filipcik@savba.sk.
Physiological research
|March 11, 2024
概括
ангиотензин转化酶2 (ACE2) 活性由 ангиотензин调节,影响SARS-CoV-2尖端蛋白结合和病毒进入. 这种相互作用可能会影响患有氨酸 - 血管新生素系统失衡的患者的COVID-19严重程度.
科学领域:
- 生物化学 生物化学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- ангиотензин转化酶2 (ACE2) 对于SARS-CoV-2感染至关重要,作为主要的病毒受体.
- ангиотензин,Ang I 和 Ang II 是 ACE2 的基质,可以影响 SARS-CoV-2 尖端蛋白结合.
研究的目的:
- 研究Ang I和Ang II对SARS-CoV-2尖端伪病毒 (PVP) 进入表达ACE2的细胞的影响.
- 探索血管酶调节病毒结合和进入的机制.
- 分析SARS-CoV-2对血管新生素代谢的影响.
主要方法:
- 在存在不同度的Ang I和Ang II的情况下,HEK-ACE2和Vero E6细胞与SARS-CoV-2Spike伪病毒 (PVP) 共同化.
- 病毒进入刺激和传染性的评估.
- 对血管酶转化酶 (ACE) 和ACE2活性进行分析.
主要成果:
- 在微分子度下,AngI和AngII显著刺激PVP的进入,AngII更强.
- 100微米的Ang II导致PVP感染率显著增加 (129.74+/-3.99%).
- 感染SARS-CoV-2导致ACE2活性降低和ACE活性增加.
- ангиотензин可以影响ACE2细胞而不涉及angiotensin I型受体.
结论:
- 假设ACE2催化口袋和SARS-CoV-2 S1结合域之间存在固体相互作用,其中基质过和增加了病毒的进入.
- 在SARS-CoV-2感染后改变的血管素代谢和ACE2/ACE活性变化是显著的.
- 这些发现与了解COVID-19患者的SARS-CoV-2入侵有关,这些患者患有影响氨酸- ангиотензин系统的并发症.
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