Nandi Seema, Sommerville Laura, Nellenbach Kimberly, Mihalko Emily, Erb Mary, Freytes Donald O, Hoffman Maureane, Monroe Dougald, Brown Ashley C
Joint Department of Biomedical Engineering, University of North Carolina at Chapel Hill and North Carolina State University, Raleigh, NC, United States; Comparative Medicine Institute, North Carolina State University, Raleigh, NC, United States.
Department of Pathology, Duke University, Durham, NC, United States.
J Colloid Interface Sci. 2020 Oct 1;577:406-418. doi: 10.1016/j.jcis.2020.05.088. Epub 2020 May 26.
Following injury, a fibrin-rich provisional matrix is formed to stem blood loss and provide a scaffold for infiltrating cells, which rebuild the damaged tissue. Defects in fibrin network formation contribute to impaired healing outcomes, as evidenced in hemophilia. Platelet-fibrin interactions greatly influence fibrin network structure via clot contraction, which increases fibrin density over time. Previously developed hemostatic platelet-like particles (PLPs) are capable of mimicking platelet functions including binding to fibrin fibers, augmenting clotting, and inducing clot retraction. In this study, we aimed to apply PLPs within a plasma-based in vitro hemophilia B model of deficient fibrin network structure to determine the ability of PLPs to improve fibrin structure and wound healing responses within hemophilia-like abnormal fibrin network formation. PLP impact on structurally deficient clot networks was assessed via confocal microscopy, a micropost deflection model, atomic force microscopy and an in vitro wound healing model of early cell migration within a provisional fibrin matrix. PLPs improved clot network density, force generation, and stiffness, and promoted fibroblast migration within an in vitro model of early wound healing under hemophilic conditions, indicating that PLPs could provide a biomimetic platform for improving wound healing events in disease conditions that cause deficient fibrin network formation.
受伤后,会形成富含纤维蛋白的临时基质以阻止失血,并为浸润细胞提供支架,这些细胞会重建受损组织。纤维蛋白网络形成缺陷会导致愈合结果受损,血友病就是明证。血小板 - 纤维蛋白相互作用通过凝块收缩极大地影响纤维蛋白网络结构,随着时间的推移,凝块收缩会增加纤维蛋白密度。先前开发的止血性类血小板颗粒(PLP)能够模拟血小板功能,包括与纤维蛋白纤维结合、增强凝血和诱导凝块回缩。在本研究中,我们旨在将PLP应用于基于血浆的纤维蛋白网络结构缺陷的体外乙型血友病模型,以确定PLP在类似血友病的异常纤维蛋白网络形成中改善纤维蛋白结构和伤口愈合反应的能力。通过共聚焦显微镜、微柱偏转模型、原子力显微镜以及临时纤维蛋白基质内早期细胞迁移的体外伤口愈合模型,评估了PLP对结构缺陷凝块网络的影响。PLP改善了凝块网络密度、力的产生和硬度,并在血友病条件下的早期伤口愈合体外模型中促进了成纤维细胞迁移,这表明PLP可以为改善导致纤维蛋白网络形成缺陷的疾病状态下的伤口愈合过程提供一个仿生平台。