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Specific Binding of Red Blood Cells to Endothelial Cells Is Regulated by Nonadsorbing Macromolecules

机译:红细胞与内皮细胞的特异性结合是由非吸附性大分子调节的。

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摘要

Abnormal adhesion of red blood cells to the endothelium has been linked to the pathophysiology of several diseases associated with vascular disorders. Various biochemical changes, including phosphatidylserine exposure on the outer membrane of red blood cells as well as plasma protein levels, have been identified as being likely to play a key role, but the detailed interplay between plasma factors and cellular factors remains unknown. It has been proposed that the adhesion-promoting effect of plasma proteins originates from ligand interaction, but evidence substantiating this assumption is often missing. In this work, we identified an alternative pathway by demonstrating that nonadsorbing macromolecules can also have a marked impact on the adhesion efficiency of red blood cells with enhanced phosphatidylserine exposure to endothelial cells. It is concluded that this adhesion-promoting effect originates from macromolecular depletion interaction and thereby presents an alternative mechanism by which plasma proteins could regulate cell-cell interactions. These findings should thus be of potential value for a detailed understanding of the pathophysiology of diseases associated with vascular complications and might be applicable to a wide range of cell-cell interactions in plasma or plasma-like media.
机译:红细胞对内皮的异常粘附与几种与血管疾病有关的疾病的病理生理学有关。各种生化变化,包括红细胞外膜上的磷脂酰丝氨酸暴露以及血浆蛋白水平,已被确定可能起关键作用,但是血浆因子和细胞因子之间的详细相互作用仍然未知。已经提出血浆蛋白的粘附促进作用源于配体相互作用,但是缺乏证实该假设的证据。在这项工作中,我们通过证明非吸附性大分子还可以通过增加磷脂酰丝氨酸对内皮细胞的暴露而对红细胞的粘附效率产生显着影响,从而找到了一条替代途径。结论是,这种促进粘附的作用源于大分子耗竭相互作用,并因此提出了血浆蛋白可以调节细胞-细胞相互作用的另一种机制。因此,这些发现对于详细了解与血管并发症有关的疾病的病理生理学具有潜在的价值,并且可能适用于血浆或血浆样介质中的多种细胞-细胞相互作用。

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