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Related Experiment Video

Updated: Sep 29, 2025

Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
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SARS-CoV-2 Spike Protein 1 Activates Microvascular Endothelial Cells and Complement System Leading to Platelet

Luca Perico1, Marina Morigi1, Miriam Galbusera1

  • 1Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.

Frontiers in Immunology
|March 24, 2022
PubMed
Summary

The SARS-CoV-2 spike protein (S1) alone can trigger inflammation and blood clots in microvasculature by activating endothelial cells via ACE2. This process, amplified by the complement system, contributes to COVID-19 complications.

Keywords:
COVID-19SARS-CoV-2 spike protein 1complement systemendothelial dysfunctioninflammationthrombosis

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Area of Science:

  • Vascular Biology
  • Immunology
  • Virology

Background:

  • Microvascular thrombosis and multiorgan failure are critical in COVID-19 mortality.
  • The role of specific SARS-CoV-2 viral elements in causing endothelial damage remains unclear.

Purpose of the Study:

  • To investigate if the SARS-CoV-2 spike protein (S1) alone can induce endothelial damage and thrombotic complications.
  • To explore the mechanisms involving ACE2, AMPK signaling, and the complement system.

Main Methods:

  • Detection of circulating S1 protein in severe COVID-19 patients' sera using ELISA.
  • In vitro studies on human microvascular endothelial cells exposed to S1 protein.
  • Analysis of adhesive molecule expression, leukocyte adhesion, platelet aggregation, ACE2, and AMPK signaling.
  • Assessment of complement activation (C3, C5b-9, C3a, C5a) and blockade experiments.

Main Results:

  • Significant S1 protein levels were detected in 30.4% of severe COVID-19 patients.
  • In vitro, S1 protein activated endothelial cells via ACE2, impairing AMPK signaling and increasing leukocyte recruitment.
  • S1 induced a pro-inflammatory phenotype with complement deposition and generation, leading to platelet aggregation.

Conclusions:

  • SARS-CoV-2-derived S1 protein is sufficient to promote inflammatory and thrombotic processes in the microvasculature.
  • The complement system amplifies these S1-induced effects, mimicking COVID-19 thromboembolic complications.
  • Blocking ACE2 or complement components can inhibit S1-induced platelet aggregation.