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SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells

Yuichiro J. Suzuki, Sofia I. Nikolaienko, Vyacheslav A. Dibrova, Yulia V. Dibrova, Volodymyr M. Vasylyk, Mykhailo Y. Novikov, Nataliia V. Shults, Sergiy G. Gychka
doi: https://doi.org/10.1101/2020.10.12.335083
Yuichiro J. Suzuki
1Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20007 USA
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Sofia I. Nikolaienko
2Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev, 01601 Ukraine
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Vyacheslav A. Dibrova
2Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev, 01601 Ukraine
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Yulia V. Dibrova
2Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev, 01601 Ukraine
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Volodymyr M. Vasylyk
3Centralized Department of Pathological Anatomy of Ivano-Frankivsk District Clinical Hospital, Ivano-Frankivsk, 76000 Ukraine
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Mykhailo Y. Novikov
4The Regional Municipal Institution «Sumy District Forensic Medical Examination Bureau», Sumy, 40050 Ukraine
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Nataliia V. Shults
1Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20007 USA
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Sergiy G. Gychka
2Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev, 01601 Ukraine
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  • For correspondence: ys82@georgetown.edu
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Abstract

Currently, the world is suffering from the pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. So far, 30 million people have been infected with SARS-CoV-2, and nearly 1 million people have died because of COVID-19 worldwide, causing serious health, economical, and sociological problems. However, the mechanism of the effect of SARS-CoV-2 on human host cells has not been defined. The present study reports that the SARS-CoV-2 spike protein alone without the rest of the viral components is sufficient to elicit cell signaling in lung vascular cells. The treatment of human pulmonary artery smooth muscle cells or human pulmonary artery endothelial cells with recombinant SARS-CoV-2 spike protein S1 subunit (Val16 – Gln690) at 10 ng/ml (0.13 nM) caused an activation of MEK phosphorylation. The activation kinetics was transient with a peak at 10 min. The recombinant protein that contains only the ACE2 receptor-binding domain of SARS-CoV-2 spike protein S1 subunit (Arg319 – Phe541), on the other hand, did not cause this activation. Consistent with the activation of cell growth signaling in lung vascular cells by SARS-CoV-2 spike protein, pulmonary vascular walls were found to be thickened in COVID-19 patients. Thus, SARS-CoV-2 spike protein-mediated cell growth signaling may participate in adverse cardiovascular/pulmonary outcomes, and this mechanism may provide new therapeutic targets to combat COVID-19.

Competing Interest Statement

The authors have declared no competing interest.

  • Abbreviations
    ACE2
    angiotensin-converting enzyme 2;
    ARDS
    acute respiratory distress syndrome;
    COVID-19
    coronavirus disease 2019;
    RBD
    receptor-binding domain;
    SARS-CoV-2
    severe acute respiratory syndrome coronavirus 2
  • Copyright 
    The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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    Posted October 12, 2020.
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    SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells
    Yuichiro J. Suzuki, Sofia I. Nikolaienko, Vyacheslav A. Dibrova, Yulia V. Dibrova, Volodymyr M. Vasylyk, Mykhailo Y. Novikov, Nataliia V. Shults, Sergiy G. Gychka
    bioRxiv 2020.10.12.335083; doi: https://doi.org/10.1101/2020.10.12.335083
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    SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells
    Yuichiro J. Suzuki, Sofia I. Nikolaienko, Vyacheslav A. Dibrova, Yulia V. Dibrova, Volodymyr M. Vasylyk, Mykhailo Y. Novikov, Nataliia V. Shults, Sergiy G. Gychka
    bioRxiv 2020.10.12.335083; doi: https://doi.org/10.1101/2020.10.12.335083

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