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在高切变率下全血中血小板、血管性血友病因子和白细胞的复杂相互作用是由血小板 GPIIb/IIIa 受体介导的。

Complex Interaction of Platelets, von Willebrand Factor and Leukocytes, in Whole Blood at High Shear Rates Is Mediated by Platelet GPIIb/IIIa Receptor.

机构信息

National Medical Research Center of Cardiology, Ministry of Health of the Russian Federation, Moscow, Russia.

出版信息

Bull Exp Biol Med. 2021 Sep;171(5):588-591. doi: 10.1007/s10517-021-05274-5. Epub 2021 Oct 7.

DOI:10.1007/s10517-021-05274-5
PMID:34618262
Abstract

We studied the contribution of von Willebrand factor (vWF) into blood cell adhesion to collagen-coated surfaces in whole blood of healthy volunteers. Adhesion of blood cells to collagen I was measured at shear rate of 2300 sec. The interaction of platelet GPIIb/IIIa receptor with vWF was blocked with monoclonal anti-GPIIb/IIIa antibodies. The degree of cell adhesion was quantified by measuring the intensity of scattered light after 15-min perfusion: in samples with blocked GPIIb/IIIa it decreased to 0.39±0.13 V vs 0.06±0.03 V in control samples (p=0.002). Under a fluorescence microscope, intensively stained structures consisting of vWF, platelets, and leukocytes attached to the collagen surface were observed. After blockade of GPIIb/IIIa, these structures were absent. Leukocyte recruitment at high shear rates is a time-dependent process sensitive to complex interaction of vWF, leukocytes, and platelets, in which the platelet GPIIb/IIIa receptor is essential.

摘要

我们研究了在健康志愿者的全血中,血管性血友病因子(vWF)对血细胞黏附到胶原蛋白涂层表面的贡献。在剪切速率为 2300 秒的情况下测量血细胞对胶原蛋白 I 的黏附。用单克隆抗 GPIIb/IIIa 抗体阻断血小板 GPIIb/IIIa 受体与 vWF 的相互作用。通过测量 15 分钟灌注后的散射光强度来定量细胞黏附程度:在阻断 GPIIb/IIIa 的样本中,其值降至 0.39±0.13 V,而在对照样本中为 0.06±0.03 V(p=0.002)。在荧光显微镜下,可以观察到强烈染色的结构,这些结构由黏附在胶原蛋白表面的 vWF、血小板和白细胞组成。阻断 GPIIb/IIIa 后,这些结构消失。白细胞在高剪切速率下的募集是一个依赖时间的过程,对 vWF、白细胞和血小板的复杂相互作用敏感,其中血小板 GPIIb/IIIa 受体是必不可少的。

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Bull Exp Biol Med. 2018 May;165(1):157-160. doi: 10.1007/s10517-018-4119-5. Epub 2018 May 24.
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von Willebrand factor and inflammation.血管性血友病因子与炎症。
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The Role of von Willebrand Factor in Vascular Inflammation: From Pathogenesis to Targeted Therapy.血管性血友病因子在血管炎症中的作用:从发病机制到靶向治疗
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