Chou Shih-Feng, Caltrider Brandon A, Azghani Ali, Neuenschwander Pierre F
Department of Mechanical Engineering, The University of Texas at Tyler, USA.
Department of Biology, The University of Texas at Tyler, USA.
Biomed J Sci Tech Res. 2020;32(3):24988-24993. doi: 10.26717/BJSTR.2020.32.005247. Epub 2020 Dec 8.
Coronary thrombosis is one of the leading causes of mortality and morbidity in cardiovascular diseases, and patients who received vascular stent treatments are likely to suffer from restenosis due to tissue damage from stenting procedures (extrinsic pathway) and/or presence of unregulated factor XII (intrinsic pathway). Regardless of the pathway, coagulation factors and exposed collagen activate the G-protein-coupled receptors located at the plasma membrane of the resting platelets resulting in the change of their shapes with protrusions of filopodia and lamellipodia for surface adhesion. In this mini review, we discussed the mechanisms involved in platelet activation, adhesion, and aggregation. More importantly, we reviewed the use of polyurethane membranes with modified surface functional groups to down-regulate platelet adhesion and aggregation activities. Polyurethane membranes with hydrophilic and negatively charged surface properties showed a reduced αIIb-β3 signaling from the activated platelets, resulting in the decrease of platelet adhesion and aggregation. The use of polyurethane membranes with modified surface properties as coatings on vascular stents provides an engineering approach to mitigate blood clotting associated with restenosis.
冠状动脉血栓形成是心血管疾病中导致死亡和发病的主要原因之一，接受血管支架治疗的患者可能会因支架置入手术造成的组织损伤（外源性途径）和/或存在不受调控的因子 XII（内源性途径）而发生再狭窄。无论哪种途径，凝血因子和暴露的胶原蛋白都会激活静息血小板质膜上的 G 蛋白偶联受体，导致其形状发生变化，出现丝状伪足和片状伪足以进行表面黏附。在这篇小型综述中，我们讨论了血小板激活、黏附和聚集所涉及的机制。更重要的是，我们回顾了使用具有修饰表面官能团的聚氨酯膜来下调血小板黏附和聚集活性的情况。具有亲水性和带负电荷表面性质的聚氨酯膜显示出活化血小板的αIIb-β3信号减少，从而导致血小板黏附和聚集减少。使用具有修饰表面性质的聚氨酯膜作为血管支架涂层提供了一种工程方法来减轻与再狭窄相关的血液凝固。
