SARS-CoV-2 刺突蛋白与 ACE2 的相互作用诱导皮质肌动蛋白的调节，包括 ERM 蛋白的去磷酸化和皮质硬度的降低。
Interaction of SARS-CoV-2 Spike protein with ACE2 induces cortical actin modulation, including dephosphorylation of ERM proteins and reduction of cortical stiffness.
机构信息
Department of Life and Environment Engineering, Faculty of Environmental Engineering, The University of Kitakyushu, 1-1 Hibikino, Wakamatsu, Kitakyushu, Fukuoka, 808-0135, Japan.
Division of Hematology and Oncology, Department of Internal Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
出版信息
Hum Cell. 2024 Oct 22;38(1):3. doi: 10.1007/s13577-024-01142-2.
Cell surface cortical actin is a regulatory target for viral infection. We aimed to investigate the effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on host cell cortical stiffness, an indicator of cortical actin structure. The receptor-binding domain (RBD) of SARS-CoV-2 Spike (S) protein induced a reduction in cortical stiffness in ACE2-expressing cells. The interaction of RBD with ACE2 caused the inactivation of Ezrin/Radixin/Moesin (ERM) proteins. We further investigated the effects of the RBD of SARS-CoV-2 Omicron variants, BA.1 and BA.5. These RBDs influenced cortical stiffness depending on their affinity for ACE2. Our study provides the first evidence that the interaction of the SARS-CoV-2 S protein with ACE2 induces mechanobiological signals and attenuates the cortical actin.
细胞表面皮质肌动蛋白是病毒感染的调节靶点。我们旨在研究严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）感染对宿主细胞皮质硬度的影响，皮质硬度是皮质肌动蛋白结构的一个指标。SARS-CoV-2 刺突（S）蛋白的受体结合域（RBD）诱导 ACE2 表达细胞的皮质硬度降低。RBD 与 ACE2 的相互作用导致 Ezrin/Radixin/Moesin（ERM）蛋白失活。我们进一步研究了 SARS-CoV-2 奥密克戎变异株 BA.1 和 BA.5 的 RBD 的影响。这些 RBD 对皮质硬度的影响取决于它们与 ACE2 的亲和力。我们的研究首次提供了证据，表明 SARS-CoV-2 S 蛋白与 ACE2 的相互作用诱导了机械生物学信号，并减弱了皮质肌动蛋白。
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