Transfusion · 2026
Endothelial thrombomodulin-Its role in trauma-induced coagulopathy.
СтатьяНазвание и аннотация: Перевод в очереди
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Abu-Hanna Jeries, Morrow Gael B, Xu Gang, Timms Lewis, Akbar Naveed, Laffan Michael, Choudhury Robin P, Curry Nicola
Аннотация
BACKGROUND: Trauma-induced coagulopathy (TIC) describes a complex set of coagulation changes affecting severely injured patients. The thrombomodulin-protein C axis is central to the evolution of TIC. Soluble thrombomodulin (sTM) levels are elevated after injury and predict poor clinical outcomes. Recently, a heritable bleeding disorder defined by injury-related excessive bleeding, markedly elevated sTM and a THBD mutation has been described. The clinical phenotype broadly mirrors that of trauma hemorrhage, and we hypothesized that their endothelial colony forming cells (ECFCs) could be used to model trauma-induced endothelial damage.
STUDY DESIGN AND METHODS: Our objectives were to: (a) define the hemostatic capacity of wild type (WT-) and THBD variant (MT-) ECFCs, using global hemostatic assays, (b) determine the hemostatic changes on ECFC surfaces after exposing cells to trauma stimuli, (c) evaluate the contributions of traumatized ECFCs and trauma patient plasma to overall hemostatic capacity, to better understand the injured endothelial-coagulation interface.
RESULTS: We show that trauma stimuli cause significant, rapid shedding of TM from WT-cells and this reduced membrane-TM supports quicker fibrinolysis and greater thrombin generating capacity. Combining trauma plasma with traumatized ECFCs attenuates and/or negates these effects.
CONCLUSION: This ECFC model provides novel mechanistic insights into TIC at the endothelial surface, informing future treatment strategies.
STUDY DESIGN AND METHODS: Our objectives were to: (a) define the hemostatic capacity of wild type (WT-) and THBD variant (MT-) ECFCs, using global hemostatic assays, (b) determine the hemostatic changes on ECFC surfaces after exposing cells to trauma stimuli, (c) evaluate the contributions of traumatized ECFCs and trauma patient plasma to overall hemostatic capacity, to better understand the injured endothelial-coagulation interface.
RESULTS: We show that trauma stimuli cause significant, rapid shedding of TM from WT-cells and this reduced membrane-TM supports quicker fibrinolysis and greater thrombin generating capacity. Combining trauma plasma with traumatized ECFCs attenuates and/or negates these effects.
CONCLUSION: This ECFC model provides novel mechanistic insights into TIC at the endothelial surface, informing future treatment strategies.