Dataset Information

Controlling Surface-Induced Platelet Activation by Agarose and Gelatin-Based Hydrogel Films.

ABSTRACT: Platelet-surface interaction is of paramount importance in biomedical applications as well as in vitro studies. However, controlling platelet-surface activation is challenging and still requires more effort as they activate immediately when contacting with any nonphysiological surface. As hydrogels are highly biocompatible, in this study, we developed agarose and gelatin-based hydrogel films to inhibit platelet-surface adhesion. We found promising agarose films that exhibit higher surface wettability, better controlled-swelling properties, and greater stiffness compared to gelatin, resulting in a strong reduction of platelet adhesion. Mechanical properties and surface wettability of the hydrogel films were varied by adding magnetite (Fe₃O₄) nanoparticles. While all of the films prevented platelet spreading, films formed by agarose and its nanocomposite repelled platelets and inhibited platelet adhesion and activation stronger than those of gelatin. Our results showed that platelet-surface activation is modulated by controlling the properties of the films underneath platelets and that the bioinert agarose can be potentially translated to the development of platelet storage and other medical applications.

SUBMITTER: Apte G

PROVIDER: S-EPMC8153948 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Controlling Surface-Induced Platelet Activation by Agarose and Gelatin-Based Hydrogel Films.

Apte Gurunath G Lindenbauer Annerose A Schemberg Jörg J Rothe Holger H Nguyen Thi-Huong TH

ACS omega 20210413 16

Platelet-surface interaction is of paramount importance in biomedical applications as well as in vitro studies. However, controlling platelet-surface activation is challenging and still requires more effort as they activate immediately when contacting with any nonphysiological surface. As hydrogels are highly biocompatible, in this study, we developed agarose and gelatin-based hydrogel films to inhibit platelet-surface adhesion. We found promising agarose films that exhibit higher surface wettab ...[more]

PMID: 34056249

Similar Datasets

Project description:Background Agonist-induced platelet activation, with the integrin αIIbβ3 conformational change, is required for fibrinogen binding. This is considered reversible under specific conditions, allowing a second phase of platelet aggregation. The signaling pathways that differentiate between a permanent or transient activation state of platelets are poorly elucidated. Objective To explore platelet signaling mechanisms induced by the collagen receptor glycoprotein VI (GPVI) or by protease-activated receptors (PAR) for thrombin that regulate time-dependent αIIbβ3 activation. Methods Platelets were activated with collagen-related peptide (CRP, stimulating GPVI), thrombin receptor-activating peptides, or thrombin (stimulating PAR1 and/or 4). Integrin αIIbβ3 activation and P-selectin expression was assessed by two-color flow cytometry. Signaling pathway inhibitors were applied before or after agonist addition. Reversibility of platelet spreading was studied by microscopy. Results Platelet pretreatment with pharmacological inhibitors decreased GPVI- and PAR-induced integrin αIIbβ3 activation and P-selectin expression in the target order of protein kinase C (PKC) > glycogen synthase kinase 3 > β-arrestin > phosphatidylinositol-3-kinase. Posttreatment revealed secondary αIIbβ3 inactivation (not P-selectin expression), in the same order, but this reversibility was confined to CRP and PAR1 agonist. Combined inhibition of conventional and novel PKC isoforms was most effective for integrin closure. Pre- and posttreatment with ticagrelor, blocking the P2Y 12 adenosine diphosphate (ADP) receptor, enhanced αIIbβ3 inactivation. Spreading assays showed that PKC or P2Y 12 inhibition provoked a partial conversion from filopodia to a more discoid platelet shape. Conclusion PKC and autocrine ADP signaling contribute to persistent integrin αIIbβ3 activation in the order of PAR1/GPVI > PAR4 stimulation and hence to stabilized platelet aggregation. These findings are relevant for optimization of effective antiplatelet treatment.

Dataset Information

Controlling Surface-Induced Platelet Activation by Agarose and Gelatin-Based Hydrogel Films.

Publications

Controlling Surface-Induced Platelet Activation by Agarose and Gelatin-Based Hydrogel Films.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets