Human blood platelets and SK-N-AS neuroblastoma cancer-cell capture at spontaneously adsorbed monolayers of fibrinogen-binding motifs, GRGDS (generic integrin adhesion), HHLGGAKQAGDV (exclusive to platelet integrin α_IIbβ₃), or octanethiol (adhesion inhibitor) at planar gold and ordered 1.6 μm diameter spherical cap gold cavity arrays were compared. In all cases, arginine/glycine/aspartic acid (RGD) promoted capture, whereas alkanethiol monolayers inhibited adhesion. Conversely only platelets adhered to alanine/glycine/aspartic acid (AGD)-modified surfaces, indicating that the AGD motif is recognized preferentially by the platelet-specific integrin, α_IIbβ₃. Microstructuring of the surface effectively eliminated nonspecific platelet/cell adsorption and dramatically enhanced capture compared to RGD/AGD-modified planar surfaces. In all cases, adhesion was reversible. Platelets and cells underwent morphological change on capture, the extent of which depended on the topography of the underlying substrate. This work demonstrates that both the nature of the modified interface and its underlying topography influence the capture of cancer cells and platelets. These insights may be useful in developing cell-based cancer diagnostics as well as in identifying strategies for the disruption of platelet cloaks around circulating tumor cells.

中文翻译：

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纤维蛋白原基序区分多肽修饰的金微孔阵列中的血小板和细胞捕获。

人血液的血小板和SK-N-AS神经母细胞瘤肿瘤细胞捕获在纤维蛋白原结合基序，GRGDS（通用整附着力），HHLGGAKQAGDV（专用于血小板整α的自发吸附单层_IIB β ₃），或辛硫醇（粘附抑制剂）在比较了平面金和直径为1.6μm的球形帽状金腔阵列。在所有情况下，精氨酸/甘氨酸/天冬氨酸（RGD）均可促进捕获，而烷硫醇单层可抑制粘附。相反地只血小板粘附到丙氨酸/甘氨酸/天冬氨酸（AGD）改性的表面，这表明AGD基序由特定血小板整联优先识别，α _IIB β ₃。与RGD / AGD修饰的平面表面相比，表面的微结构有效消除了非特异性血小板/细胞的吸附，并大大提高了捕获率。在所有情况下，粘附都是可逆的。血小板和细胞在捕获时会发生形态变化，其程度取决于下层底物的形貌。这项工作表明，修改后的界面的性质及其潜在的地形都会影响癌细胞和血小板的捕获。这些见解可能有助于开发基于细胞的癌症诊断方法，以及确定破坏循环肿瘤细胞周围血小板隐身物的策略。