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首页> 外文期刊>Acta biomaterialia >Elucidation of adhesion-dependent spontaneous apoptosis in macrophages using phase separated PEG/polyurethane films
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Elucidation of adhesion-dependent spontaneous apoptosis in macrophages using phase separated PEG/polyurethane films

机译：使用相分离的PEG /聚氨酯薄膜阐明巨噬细胞中黏附依赖性自发凋亡

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摘要

Circulating monocytes undergo spontaneous apoptosis when there is no activation stimulus, which is critical to population control for proper host response to implants. As activation and apoptosis of monocytes/macrophages are regulated by cell-cell and cell-matrix interactions, their regulatory mechanism was investigated in this study using polyethylene glycol (PEG)-containing polyurethane films in which PEG-rich and polyester-rich domains were phase separated. Human blood monocyte-derived macrophages (HBMs) preferentially adhered to PEG domains (cell-matrix interaction) due to the low molecular weight (600 g mol-1), resulting in increased HBM density (cell-cell interaction). As both cell-cell and cell-matrix interactions were promoted, HBM apoptosis increased, while their activation as measured by phagocytosis, intracellular reactive oxygen species (ROS) level and matrix metalloproteinase-9 production decreased compared to PEG-free films. When cell seeding density and cell-Adhesive gelatin coating on silicone films were controlled, a cooperative role of cell-matrix (adhesion) and cell-cell (density) interactions in inducing HBM apoptosis was observed. Expression of the macrophage adhesion molecule CD11b caused apoptosis in this context, which was mediated by tissue necrosis factor-?? signaling but down-regulated by the ROS inhibitor diphenylene iodonium and the anti-inflammatory peptide Ac-SDKP, suggesting a new concept for the design of biomaterials that allows for cell adhesion without excessive inflammatory activation. ? 2012 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
机译：没有激活刺激时，循环单核细胞会自发凋亡，这对于控制宿主对植入物的适当反应至关重要。由于单核细胞/巨噬细胞的活化和凋亡受细胞与细胞和细胞-基质相互作用的调节，因此在本研究中，我们使用含聚乙二醇（PEG）和富聚酯结构域为相的含聚乙二醇（PEG）的聚氨酯薄膜研究了它们的调节机制。分开。人血单核细胞衍生的巨噬细胞（HBM）由于分子量低（600 g mol-1）而优先粘附到PEG域（细胞-基质相互作用），导致HBM密度增加（细胞-细胞相互作用）。与无PEG膜相比，随着细胞-细胞和细胞-基质相互作用的促进，HBM细胞凋亡增加，而其吞噬作用，细胞内活性氧（ROS）水平和基质金属蛋白酶9产生的活化降低。当控制细胞播种密度和在硅膜上的细胞粘附明胶涂层时，观察到细胞基质（粘附）和细胞-细胞（密度）相互作用在诱导HBM细胞凋亡中的协同作用。在这种情况下，巨噬细胞粘附分子CD11b的表达引起细胞凋亡，这是由组织坏死因子-β介导的。信号但被ROS抑制剂二亚苯基碘鎓和抗炎肽Ac-SDKP下调，为生物材料设计提出了一个新概念，该概念允许细胞粘附而无需过度的炎症激活。 ？ 2012年Acta Materialia Inc.由Elsevier Ltd.发行。保留所有权利。

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