Tackling the Root Cause of Surface-Induced Coagulation: Inhibition of FXII Activation to Mitigate Coagulation Propagation and Prevent Clotting.
C1-esterase-inhibitor
FXII activation
hemocompatibility
hemocompatible surface modification
polymer brushes
β-FXIIa
Journal
Macromolecular bioscience
ISSN: 1616-5195
Titre abrégé: Macromol Biosci
Pays: Germany
ID NLM: 101135941
Informations de publication
Date de publication:
24 Sep 2023
24 Sep 2023
Historique:
revised:
01
09
2023
received:
10
07
2023
pubmed:
24
9
2023
medline:
24
9
2023
entrez:
24
9
2023
Statut:
aheadofprint
Résumé
Factor XII (FXII) is a zymogen present in blood that tends to adsorb onto the surfaces of blood-contacting medical devices. Once adsorbed, it becomes activated, initiating a cascade of enzymatic reactions that lead to surface-induced coagulation. This process is characterized by multiple redundancies, making it extremely challenging to prevent clot formation and preserve the properties of the surface. In this study, a novel modulatory coating system based on C1-esterase inhibitor (C1INH) functionalized polymer brushes, which effectively regulates the activation of FXII is proposed. Using surface plasmon resonance it is demonstrated that this coating system effectively repels blood plasma proteins, including FXII, while exhibiting high activity against activated FXII and plasma kallikrein under physiological conditions. This unique property enables the modulation of FXII activation without interfering with the overall hemostasis process. Furthermore, through dynamic Chandler loop studies, it is shown that this coating significantly improves the hemocompatibility of polymeric surfaces commonly used in medical devices. By addressing the root cause of contact activation, the synergistic interplay between the antifouling polymer brushes and the modulatory C1INH is expected to lay the foundation to enhance the hemocompatibility of medical device surfaces.
Identifiants
pubmed: 37742317
doi: 10.1002/mabi.202300321
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2300321Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : 346972946
Organisme : Deutsche Forschungsgemeinschaft
ID : 640574
Organisme : German Federal Ministry of Education and Research
ID : 031B1153A
Organisme : German Federal Ministry of Education and Research
ID : 031B1154B
Informations de copyright
© 2023 The Authors. Macromolecular Bioscience published by Wiley-VCH GmbH.
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