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An In Vitro 3D Model and Computational Pipeline to Quantify the Vasculogenic Potential of iPSC-Derived Endothelial Progenitors
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SARS-CoV-2 spike protein induces endothelial dysfunction in 3D engineered vascular networks
Biorxiv : the Preprint Server for Biology
|October 14, 2022
Summary
This study developed a 3D in vitro model using stem cell-derived endothelial cells to investigate COVID-19's effects. The model successfully replicated SARS-CoV-2 spike protein-induced endothelial dysfunction and showed dexamethasone could prevent it.
Area of Science:
- Cardiovascular Biology
- Infectious Disease Research
- Stem Cell Biology
Background:
- Long-term impacts of COVID-19 necessitate better in vitro models for understanding pathogenicity.
- Endothelial dysfunction is a key feature of severe COVID-19, impacting organ function.
Approach:
- Developed a 3D in vitro model using induced pluripotent stem cell-derived endothelial progenitors in collagen hydrogels.
- Treated the model with SARS-CoV-2 spike protein to mimic COVID-19 effects on the endothelium.
- Utilized dexamethasone to assess its potential in preventing SARS-CoV-2-induced endothelial dysfunction.
Key Points:
- SARS-CoV-2 spike protein significantly reduced vessel formation and network connectivity in the endothelial model.
- Dexamethasone treatment successfully prevented spike protein-induced endothelial dysfunction.
- The model confirmed the release of inflammatory cytokines linked to the COVID-19 cytokine storm.
Conclusions:
- This 3D in vitro angiogenesis model effectively reproduces COVID-19-induced endothelial dysfunction, even without immune cells.
- The model serves as a valuable tool for studying COVID-19's vascular impact and testing therapeutic interventions.
- Findings highlight the critical role of endothelial cells in COVID-19 pathogenesis and potential treatment strategies.
