Jiang Peipei, Bian Maohong, Ma Wenjuan, Liu Chunqiu, Yang Peng, Zhu Bangqiang, Xu Yuanhong, Zheng Meijuan, Qiao Jinpin, Shuai Zongwen, Zhou Xueyong, Huang Dake
Department of Blood Transfusion, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Cell Physiol Biochem. 2016;40(6):1391-1400. doi: 10.1159/000453191. Epub 2016 Dec 19.
The progression of systemic lupus erythematosus (SLE) leads to anemia in patients, adversely affecting prognosis. The diverse causes of anemia may include excessive eryptosis or premature suicidal erythrocyte death characterized by cell shrinkage and phosphatidylserine (PS) exposure on the cell surface. The present study explored if SLE enhances eryptosis and the underlying mechanisms.
Eryptosis was assessed using flow cytometry in healthy volunteers (n = 20) and anemic patients hospitalized for SLE (n = 22), for parameters including PS exposure, cell volume, cytosolic calcium ion (Ca2+) levels and reactive oxygen species (ROS) and ceramide abundance. These indicators were measured in erythrocytes of experimental subjects and erythrocytes treated with plasma from healthy volunteers or SLE patients.
The hemoglobin and hematocrit levels were significantly lower in anemic SLE patients than in healthy volunteers (***p<0.001, p<0.001, respectively). The percentage of PS-exposing erythrocytes was significantly higher in SLE patients than in healthy volunteers (p<0.001), accompanied by an increase in cytosolic Ca2+ levels, oxidative stress. The measurements of PS and Ca2+ levels were significantly higher in the erythrocytes of healthy volunteers following incubation in plasma of SLE patients than in plasma of healthy volunteers for 24h (***p<0.001, *p<0.05 respectively).
Eryptosis is enhanced in SLE and may contribute to anemia. The probable underlying mechanisms may be an excessive formation of ROS in erythrocytes. Also, some plasma components may trigger eryptosis by increasing the cytosolic Ca2+ concentration.
系统性红斑狼疮（SLE）的进展会导致患者贫血，对预后产生不利影响。贫血的多种原因可能包括红细胞凋亡增加或过早的自杀性红细胞死亡，其特征为细胞萎缩和细胞表面磷脂酰丝氨酸（PS）暴露。本研究探讨了SLE是否会增强红细胞凋亡及其潜在机制。
使用流式细胞术评估20名健康志愿者和22名因SLE住院的贫血患者的红细胞凋亡情况，检测参数包括PS暴露、细胞体积、胞质钙离子（Ca2+）水平、活性氧（ROS）以及神经酰胺丰度。在实验对象的红细胞以及用健康志愿者或SLE患者血浆处理过的红细胞中测量这些指标。
贫血SLE患者的血红蛋白和血细胞比容水平显著低于健康志愿者（分别为p<0.001，p<0.001）。SLE患者中PS暴露的红细胞百分比显著高于健康志愿者（p<0.001），同时伴有胞质Ca2+水平升高和氧化应激增加。健康志愿者的红细胞在SLE患者血浆中孵育24小时后，PS和Ca2+水平的测量值显著高于在健康志愿者血浆中的测量值（分别为p<0.001，*p<0.05）。
SLE中红细胞凋亡增强，可能导致贫血。潜在机制可能是红细胞中ROS过度形成。此外，一些血浆成分可能通过增加胞质Ca2+浓度触发红细胞凋亡。
