Hyperadhesive von Willebrand Factor Promotes Extracellular Vesicle-Induced Angiogenesis: Implication for LVAD-Induced Bleeding

Bleeding associated with left ventricular assist device (LVAD) implantation has been attributed to the loss of large von Willebrand factor (VWF) multimers to excessive cleavage by ADAMTS-13, but this mechanism is not fully supported by the current evidence. We analyzed VWF reactivity in longitudinal...

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Detalles Bibliográficos
Autores principales: Yang, Mengchen, Houck, Katie L., Dong, Xinlong, Hernandez, Maria, Wang, Yi, Nathan, Sriram S., Wu, Xiaoping, Afshar-Kharghan, Vahid, Fu, Xiaoyun, Cruz, Miguel A., Zhang, Jianning, Nascimbene, Angelo, Dong, Jing-fei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Preclinical Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8993768/
https://www.ncbi.nlm.nih.gov/pubmed/35411318
http://dx.doi.org/10.1016/j.jacbts.2021.12.005
Descripción
Sumario:Bleeding associated with left ventricular assist device (LVAD) implantation has been attributed to the loss of large von Willebrand factor (VWF) multimers to excessive cleavage by ADAMTS-13, but this mechanism is not fully supported by the current evidence. We analyzed VWF reactivity in longitudinal samples from LVAD patients and studied normal VWF and platelets exposed to high shear stress to show that VWF became hyperadhesive in LVAD patients to induce platelet microvesiculation. Platelet microvesicles activated endothelial cells, induced vascular permeability, and promoted angiogenesis in a VWF-dependent manner. Our findings suggest that LVAD-driven high shear stress primarily activates VWF, rather than inducing cleavage in the majority of patients.

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