Platelet Extracellular Vesicles Restore Plasma Membrane Integrity Following Endothelial Cell Trauma
Seitz, Taylor
Seitz, Taylor
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Abstract
Hemostasis requires the rapid transformation of vascular endothelium into a pro-coagulant, repair competent surface following injury, a process critically dependent on phosphatidylserine (PS) externalization. In traumatic injury, extracellular histones disrupt endothelial plasma membranes and induce calcium influx, creating a need for efficient membrane repair to preserve vascular integrity. While prior work demonstrated that histone-induced membrane permeabilization is transient, unlike sustained ionomycin-induced calcium influx, and that extracellular calcium modulates histone membrane interactions by screening negatively charged phospholipids; the mechanisms governing endothelial recovery remain incompletely understood. We investigated endothelial membrane repair following histone-mediated injury, with a focus on the interplay between calcium signaling and extracellular vesicle (EV) uptake. Using endothelial cell models, we demonstrate that low extracellular calcium enhances histone-membrane interactions, leading to increased cytotoxicity and membrane disruption. Building on this, we quantified membrane repair kinetics under varying conditions and assessed the contribution of plasma and platelet extracellular vesicles. Our findings reveal that blood products significantly enhance endothelial recovery compared to standard media conditions. Notably, EVs promote membrane repair efficiency and restore membrane integrity following injury, suggesting an active role in endothelial healing. These results support the hypothesis that circulating EVs function as mediators of vascular repair in addition to their established roles in coagulation. Collectively, this work identifies extracellular vesicles as key contributors to endothelial membrane repair following traumatic injury and highlights a potential therapeutic application for EV-based interventions in vascular damage. Ongoing studies are exploring how TMEM16F, a related phospholipid scrambling protein, integrates with EV-driven repair processes to coordinate endothelial recovery and hemostatic function.
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Date
1/1/2026
Student Status
Junior (Graduating in 2027)
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Poster
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Biomedical Engineering
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College of Engineering and Mathematical Sciences
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Clinical Science