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Author Spotlight: A Multi-Depth Porcine Model for Comprehensive Study of Burn Injuries and Healing Processes
Published on: February 23, 2024
Plasmas From Patients With Burn Injury Induce Endotheliopathy Through Different Pathways
John W Keyloun1, Edward J Kelly1, Bonnie C Carney2
1The Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, District of Columbia; Firefighters' Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, District of Columbia.
Burn patient plasma variably disrupts endothelial barrier function, increasing permeability. Higher syndecan-1 levels correlate with this effect, though apoptosis and gap size changes don't fully explain the permeability alterations in burn shock.
Area of Science:
- Vascular Biology
- Burn Injury Pathophysiology
- Endothelial Function
Background:
- Endothelial injury's role in burn shock is unclear.
- Burn patient plasmas may dysregulate endothelial barrier function.
Purpose of the Study:
- Investigate mechanisms of endothelial barrier dysfunction in burn shock.
- Assess the impact of burn patient plasma on endothelial cells.
Main Methods:
- Collected plasma from burn patients (n=8) within 4 hours of admission.
- Exposed human umbilical vein endothelial cell monolayers (HUVEC-m) to patient or control plasma.
- Assessed HUVEC-m permeability, intercellular gap area, apoptosis, and gene expression.
Main Results:
- Five patient plasmas significantly increased HUVEC-m permeability.
- Higher syndecan-1 levels were observed in plasmas that increased permeability.
- Intercellular gap area and apoptosis increased, but did not fully correlate with permeability changes.
Conclusions:
- Burn patient plasmas variably disrupt endothelial cell homeostasis.
- Increased permeability, gap area, and apoptosis are observed but not fully explained by gap size or apoptosis alone.
- Syndecan-1 may play a role in burn-induced endothelial barrier dysfunction.
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