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Ceramide in suicidal death of erythrocytes

机译：神经酰胺在红细胞自杀性死亡中的作用

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The suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling resulting in phosphatidylserine exposure at the cell surface. Eryptosis is stimulated in a wide variety of diseases including sepsis, haemolytic uremic syndrome, malaria, sickle-cell anemia, beta-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency and Wilson's disease. Moreover, eryptosis is elicited by osmotic shock, oxidative stress, energy depletion as well as a wide variety of endogenous mediators and xenobiotics. Excessive eryptosis is observed in erythrocytes lacking the cGMP-dependent protein kinase type I (cGKI) or the AMP-activated protein kinase AMPK. Inhibitors of eryptosis include erythropoietin, nitric oxide NO, catecholamines and high concentrations of urea. Eryptosis-triggering diseases and chemicals are partially effective by stimulating the formation of ceramide, which in turn fosters cell membrane scrambling. Accordingly, ceramide-induced eryptosis participates in the pathophysiology of several diseases and contributes to the effects of a large number of xenobiotics. The mechanisms underlying ceramide formation in erythrocytes are, however, still ill defined. In case of osmotic cell shrinkage, ceramide formation is apparently due to activation of phospholipase 2, leading to formation of platelet activating factor PAF and PAF-dependent stimulation of ceramide formation, which possibly involves acid sphingomyelinase. Additional experiments are needed to conclusively define the ceramide-generating enzyme and the ceramide-dependent cellular events eventually leading to suicidal erythrocyte death.
机译：红细胞的自杀死亡或隐匿性特征在于细胞萎缩，膜起泡和细胞膜磷脂加扰，导致磷脂酰丝氨酸暴露于细胞表面。在多种疾病中会刺激隐匿性疾病，包括败血症，溶血性尿毒症综合征，疟疾，镰状细胞性贫血，β-地中海贫血，葡萄糖-6-磷酸脱氢酶（G6PD）缺乏，磷酸盐消耗，铁缺乏和威尔逊氏病。此外，通过渗透压休克，氧化应激，能量耗竭以及各种内源性介体和异种生物引起隐匿性。在缺少cGMP依赖型I蛋白激酶（cGKI）或AMP激活的蛋白激酶AMPK的红细胞中观察到过度的加密。隐匿性抑制剂包括促红细胞生成素，一氧化氮NO，儿茶酚胺和高浓度尿素。通过刺激神经酰胺的形成，触发密码病的疾病和化学物质在某种程度上是有效的，从而促进了细胞膜的争夺。因此，神经酰胺诱导的隐性参与多种疾病的病理生理学，并有助于大量异种生物的作用。然而，在红细胞中神经酰胺形成的基础机制仍不清楚。在渗透性细胞收缩的情况下，神经酰胺的形成显然是由于磷脂酶2的活化，导致血小板活化因子PAF的形成和神经酰胺形成的PAF依赖性刺激，这可能涉及酸性鞘磷脂酶。需要额外的实验来最终确定神经酰胺生成酶和神经酰胺依赖性细胞事件，最终导致自杀性红细胞死亡。

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