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• W4387592319 endingPage "646" @default.
• W4387592319 startingPage "639" @default.
• W4387592319 abstract "Major traumatic injury is associated with early hemorrhage-related and late-stage deaths due to multiple organ failure (MOF). While improvements to hemostatic resuscitation have significantly reduced hemorrhage-related deaths, the incidence of MOF among trauma patients remains high. Dysregulation of vascular endothelial cell (EC) barrier function is a central mechanism in the development of MOF; however, the mechanistic triggers remain unknown. Accelerated fibrinolysis occurs in a majority of trauma patients, resulting in high circulating levels of fibrin(ogen) degradation products, such as fragment X. To date, the relationship between fragment X and EC dysregulation and barrier disruption is unknown. The goal of this study was to determine the effects of fragment X on EC barrier integrity and expression of paracellular junctional proteins that regulate barrier function.Human lung microvascular endothelial cells (HLMVECs) were treated with increasing concentrations of fragment X (1, 10, and 100 μg/mL), and barrier function was monitored using the xCELLigence live-cell monitoring system. Quantitative PCR (qPCR) was performed to measure changes in EC expression of 84 genes. Immunofluorescent (IF) cytostaining was performed to validate qPCR findings.Fragment X treatment significantly increased endothelial permeability over time (P < 0.05). There was also a significant reduction in VE-cadherin mRNA expression in fragment X-treated HLMVECs compared to control (P = 0.01), which was confirmed by IF staining.Fragment X may induce EC hyperpermeability by reducing VE-cadherin expression. This suggests that a targeted approach to disrupting EC-fragment X interactions could mitigate EC barrier disruption, organ edema, and MOF associated with major trauma." @default.
• W4387592319 created "2023-10-13" @default.
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• W4387592319 date "2024-01-01" @default.
• W4387592319 modified "2023-10-16" @default.
• W4387592319 title "Fibrinogen Fragment X Mediates Endothelial Barrier Disruption via Suppression of VE-Cadherin" @default.
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• W4387592319 doi "https://doi.org/10.1016/j.jss.2023.09.027" @default.
• W4387592319 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37837820" @default.
• W4387592319 hasPublicationYear "2024" @default.
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