A Flow Induced Autoimmune Response and Accelerated Senescence of Red Blood Cells in Cardiovascular Devices
A Flow Induced Autoimmune Response and Accelerated Senescence of Red Blood Cells in Cardiovascular Devices
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DOI：
10.1038/s41598-019-55924-y
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发表时间：
2019-12-19
影响因子：
4.6
通讯作者：
O'Rear, Edgar A.
中科院分区：
文献类型：
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作者：
Buerck, James P.;Burke, Dustin K.;O'Rear, Edgar A.
通过心脏泵、人工心脏瓣膜和其他心血管装置的红细胞（rbc）由于非生理性力量而经历早期衰老。我们假设机械性创伤通过膜蛋白变形导致自然产生的IgG结合而加速衰老。从健康志愿者血液中分离的红细胞在粘度计或微流体通道中暴露于高剪切应力下，以模拟机械损伤，然后与自体血浆孵育。观察到IgG结合增加，表明力导致暴露表位的膜蛋白构象改变，表位可能是带3的衰老细胞抗原。免疫球蛋白的结合提示其在脾脏红细胞的早期隔离和吞噬中起作用。IgG的测量有望作为预示心血管患者并发症的标志，并作为改进医疗设备设计的一种手段，在这些设备中，红细胞易受亚致死创伤。
Red blood cells (RBCs) passing through heart pumps, prosthetic heart valves and other cardiovascular devices undergo early senescence attributed to non-physiologic forces. We hypothesized that mechanical trauma accelerates aging by deformation of membrane proteins to cause binding of naturally occurring IgG. RBCs isolated from blood of healthy volunteers were exposed to high shear stress in a viscometer or microfluidics channel to mimic mechanical trauma and then incubated with autologous plasma. Increased binding of IgG was observed indicating forces caused conformational changes in a membrane protein exposing an epitope(s), probably the senescent cell antigen of band 3. The binding of immunoglobulin suggests it plays a role in the premature sequestration and phagocytosis of RBCs in the spleen. Measurement of IgG holds promise as a marker foreshadowing complications in cardiovascular patients and as a means to improve the design of medical devices in which RBCs are susceptible to sublethal trauma.