Institute for Laboratory and Transfusion Medicine, University of Regensburg, Regensburg, Germany.
Transfusion. 2013 Mar;53(3):612-26. doi: 10.1111/j.1537-2995.2012.03775.x. Epub 2012 Jul 15.
Stored platelet concentrates (PLCs) for transfusion develop a platelet storage lesion (PSL), resulting in decreased platelet (PLT) viability and function. The processes leading to PSL have not been described in detail and no data describe molecular changes occurring in all three components of stored PLCs: PLTs, PLC extracellular vesicles (PLC-EVs), and plasma.
Fifty PLCs from healthy individuals were stored under standard blood banking conditions for 5 days. Changes in cholesterol, glycerophospholipid, and sphingolipid species were analyzed in PLTs, PLC-EVs, and plasma by mass spectrometry and metabolic labeling. Immunoblots were performed to compare PLT and PLC-EV protein expression.
During 5 days, PLTs transferred glycerophospholipids, cholesterol, and sphingolipids to newly formed PLC-EVs, which increased corresponding lipids by 30%. Stored PLTs significantly increased ceramide (Cer; +53%) and decreased sphingosine-1-phosphate (-53%), shifting sphingolipid metabolism toward Cer. In contrast, plasma accumulated minor sphingolipids. Compared to PLTs, fresh PLC-EVs were enriched in lysophosphatidic acid (60-fold) and during storage showed significant increases in cholesterol, sphingomyelin, dihydrosphingomyelin, plasmalogen, and lysophosphatidylcholine species, as well as accumulation of apolipoproteins A-I, E, and J/clusterin.
This is the first detailed analysis of lipid species in all PLC components during PLC storage, which might reflect mechanisms active during in vivo PLT senescence. Stored PLTs reduce minor sphingolipids and shift sphingolipid metabolism toward Cer, whereas in the plasma fraction minor sphingolipids increase. The composition of PLC-EVs resembles that of lipid rafts and confirms their role as carriers of bioactive molecules and master regulators in vascular disease.
储存的血小板浓缩物（PLC）在输血过程中会发生血小板储存损伤（PSL），导致血小板（PLT）活力和功能下降。导致 PSL 的过程尚未详细描述，也没有数据描述储存的 PLC 中所有三个成分（PLT、PLC 细胞外囊泡（PLC-EV）和血浆）中发生的分子变化。
将 50 个来自健康个体的 PLC 在标准血库条件下储存 5 天。通过质谱和代谢标记分析 PLT、PLC-EV 和血浆中的胆固醇、甘油磷脂和鞘脂种类的变化。进行免疫印迹以比较 PLT 和 PLC-EV 蛋白表达。
在 5 天内，PLT 将甘油磷脂、胆固醇和鞘脂转移到新形成的 PLC-EV 中，使相应的脂质增加了 30%。储存的 PLT 显著增加了神经酰胺（Cer；+53%）并减少了鞘氨醇-1-磷酸（-53%），使鞘脂代谢向 Cer 转移。相比之下，血浆中积累了少量的鞘脂。与 PLT 相比，新鲜的 PLC-EV 富含溶血磷脂酸（60 倍），在储存过程中，胆固醇、鞘磷脂、二氢鞘磷脂、溶血磷脂酰胆碱和神经鞘磷脂等种类显著增加，载脂蛋白 A-I、E 和 J/类载脂蛋白增加。
这是首次对 PLC 储存过程中所有 PLC 成分中的脂质种类进行详细分析，可能反映了体内 PLT 衰老过程中的活跃机制。储存的 PLT 减少了少量的鞘脂，并使鞘脂代谢向 Cer 转移，而在血浆部分则增加了少量的鞘脂。PLC-EV 的组成类似于脂筏，证实了它们作为生物活性分子载体和血管疾病主要调节剂的作用。
