Zia Fatima, Kendall Michaela, Watson Steve P, Mendes Paula M
School of Chemical Engineering, College of Engineering and Physical Sciences, University of Birmingham B15 2TT, UK. Email:
Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, The Midlands, UK.
RSC Adv. 2018 Nov 12;8(66):37789-37794. doi: 10.1039/c8ra07315e.
Nanoparticles are key components underlying recent technological advances in various industrial and medical fields, and thus understanding their mode of interaction with biological systems is essential. However, while several nanoparticle systems have been shown to interact with blood platelets, many questions remain concerning the mechanisms of platelet activation and the role that the physicochemical properties of nanoparticles play in inducing platelet aggregation. Here, using negatively charged polystyrene nanoparticles with sizes of 25, 50, 119, 151, 201 nm and negatively charged platinum nanoparticles with sizes of 7 and 73 nm, we show that it is not the size of the nanoparticles but rather the nanoparticle surface area that is critical in mediating the effects on platelet activation. The nanoparticles stimulate platelet aggregation through passive (agglutination) and activation of integrin αIIbβ3 through a pathway regulated by Src and Syk tyrosine kinase.
纳米颗粒是近期各工业和医学领域技术进步的关键组成部分，因此了解它们与生物系统的相互作用模式至关重要。然而，虽然已有几种纳米颗粒系统被证明可与血小板相互作用，但关于血小板激活机制以及纳米颗粒的物理化学性质在诱导血小板聚集过程中所起的作用，仍存在许多问题。在此，我们使用尺寸为25、50、119、151、201 nm的带负电荷的聚苯乙烯纳米颗粒以及尺寸为7和73 nm的带负电荷的铂纳米颗粒，证明介导对血小板激活影响的关键因素不是纳米颗粒的大小，而是纳米颗粒的表面积。纳米颗粒通过被动（凝集）以及经由Src和Syk酪氨酸激酶调节的途径激活整合素αIIbβ3来刺激血小板聚集。
