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血浆中非吸附性大分子诱导红细胞黏附于内皮细胞。

Non-adsorbing macromolecules in plasma induce erythrocyte adhesion to the endothelium.

机构信息

School of Chemical and Biomedical Engineering, Nanyang Technological University, 70 Nanyang Drive, 639798, Singapore.

出版信息

Chemphyschem. 2011 Nov 18;12(16):2989-94. doi: 10.1002/cphc.201100471. Epub 2011 Oct 13.

Abstract

Red blood cell (RBC) adhesion to the endothelium is usually insignificant. However, an enhanced adhesion can be observed in various pathological conditions such as diabetes mellitus or sickle cell disease, which is often accompanied by elevated levels of pro-adhesive plasma proteins such as fibrinogen. In the past, these proteins have only been considered to act as ligands, cross-linking the corresponding receptors on adjacent cells, but the detailed underlying mechanism often remained obscure. This work demonstrates that the presence of non-adsorbing polymers in plasma can also enhance the adhesion efficiency of RBCs to endothelial cells (ECs) through depletion interaction. Furthermore, adhesion of RBCs to ECs may be likewise promoted by the protein fibrinogen through depletion interaction. We propose an alternative mechanism for the pro-adhesive effects of plasma proteins and indicate that depletion interaction might play a significant role for the stabilization and destabilization of blood flow in health and disease.

摘要

红细胞(RBC)与内皮细胞的黏附通常可以忽略不计。然而,在某些病理情况下,如糖尿病或镰状细胞病,这种黏附作用会增强,同时伴有促黏附血浆蛋白(如纤维蛋白原)水平的升高。过去,这些蛋白质仅被认为作为配体起作用,交联相邻细胞上相应的受体,但详细的潜在机制通常仍不清楚。本研究表明,血浆中存在不吸附的聚合物也可以通过耗竭相互作用增强 RBC 与内皮细胞(EC)的黏附效率。此外,纤维蛋白原等蛋白质也可以通过耗竭相互作用促进 RBC 与 EC 的黏附。我们提出了一种解释血浆蛋白促黏附作用的替代机制,并指出耗竭相互作用可能在健康和疾病中对血流的稳定和不稳定起着重要作用。

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