牛红细胞对病理生理促凋亡刺激的反应性死亡检测。
Examination of Bovine Red Blood Cell Death in Response to Pathophysiologic Proapoptotic Stimuli.
机构信息
Applied Bioscience Program, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.
Faculty of Health Sciences, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.
出版信息
Front Biosci (Landmark Ed). 2023 Dec 6;28(12):331. doi: 10.31083/j.fbl2812331.
BACKGROUND
Interspecies variations in mammalian red blood cells (RBCs) are observed in circulating RBC lifespan, cell size, fluidity, aggregation, water permeability, metabolism, lipid composition, and the overall proteome. Bovine RBC cell membrane is deficient in phosphatidylcholine and exhibits anomalies in the arrangement of phosphatidylethanolamine within the lipid bilayer. However, like human RBCs, virtually all the aminophospholipid phosphatidylserine (PS) is found within the cytoplasmic side of the cell membrane of intact circulating bovine RBCs. During apoptotic cell death of human and murine RBCs, PS translocates to the outer leaflet of the cell membrane via Ca2+-dependent and -independent signaling mechanisms. However, little is known about this process in bovine RBCs.
METHODS
Using cytofluorometry analyses, we characterized and compared the cell death responses in bovine and human RBCs exposed to various pathophysiologic cell stressors.
RESULTS
Ionic stress, by ionophore treatment, and oxidative stress enhanced cytoplasmic Ca2+ levels and cell membrane PS expression in both bovine and human RBCs. Fever-grade hyperthermia and energy starvation promoted Ca2+ influx and elevated reactive oxygen species levels in both human and bovine RBCs. However, bovine RBCs displayed minimal increases in PS expression elicited by hyperthermia, energy starvation, and extracellular hypertonicity as compared to human RBCs. In response to decreased extracellular osmolality, bovine RBCs exhibited significantly enhanced fragility as compared to human RBCs.
CONCLUSIONS
Bovine RBCs display differential cell death patterns as compared to human RBCs, only partly explained by increased Ca2+ influx and oxidative stress. Premature removal of circulating RBCs could potentially contribute to the pathogenesis of anemia in cattle caused by a wide range of factors such as systemic diseases, parasitic infections, and nutritional deficiencies.
背景
在哺乳动物的红细胞（RBC）中，循环 RBC 寿命、细胞大小、流动性、聚集、水通透性、代谢、脂质组成和整体蛋白质组中都存在种间差异。牛 RBC 细胞膜缺乏磷脂酰胆碱，并表现出磷脂酰乙醇胺在脂质双层内排列的异常。然而，与人类 RBC 一样，完整循环牛 RBC 细胞膜的细胞质侧几乎所有的氨基磷脂磷脂酰丝氨酸（PS）都存在。在人类和鼠类 RBC 的凋亡性细胞死亡过程中，PS 通过 Ca2+依赖性和非依赖性信号机制转移到细胞膜的外叶。然而，关于牛 RBC 中的这一过程知之甚少。
方法
使用细胞荧光分析，我们对暴露于各种病理生理细胞应激源的牛和人 RBC 的细胞死亡反应进行了特征描述和比较。
结果
离子载体处理的离子应激和氧化应激增强了牛和人 RBC 的细胞质 Ca2+水平和细胞膜 PS 表达。发热级别的高热和能量饥饿促进了人 RBC 和牛 RBC 中的 Ca2+内流和活性氧水平的升高。然而，与人类 RBC 相比，高热、能量饥饿和细胞外高渗性引起的 PS 表达增加在牛 RBC 中仅略有增加。与人类 RBC 相比，牛 RBC 在响应细胞外渗透压降低时表现出明显增强的脆性。
结论
与人类 RBC 相比，牛 RBC 显示出不同的细胞死亡模式，这部分归因于 Ca2+内流和氧化应激的增加。循环 RBC 的过早清除可能有助于由多种因素引起的牛贫血的发病机制，这些因素包括全身性疾病、寄生虫感染和营养缺乏等。
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