The clearance mechanism of chilled blood platelets
The clearance mechanism of chilled blood platelets
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DOI：
10.1016/s0092-8674(02)01253-9
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发表时间：
2003-01-10
期刊：
影响因子：
64.5
通讯作者：
Hartwig, JH
中科院分区：
文献类型：
--
作者：
Hoffmeister, KM;Felbinger, TW;Hartwig, JH
输注血小板是一种非常常见的救命医疗程序。并不广为人知的是，与其他血细胞不同的是，如果在输血前冷藏，血小板会迅速离开血液循环。这一特点要求血液服务机构在室温下储存血小板，限制了临床需要的血小板供应。在这里，我们描述这个清除系统的机制，这是一个长期存在的谜团。冷冻血小板聚集其von Willebrand(VWF)受体，通过肝脏巨噬细胞补体3型(CR3)受体诱导对小鼠和人类血小板的识别。CR3表达但不表达CR3缺陷的小鼠暴露在寒冷环境中会迅速降低血小板数量。为激活血小板做好冷却准备。我们认为，血小板是温度传感器，启动于周围部位，在整个进化过程中，大多数损伤都发生在那里。清除可通过激活血小板来防止病理性血栓形成。冷冻后的血小板与VWF结合，输注CR3缺陷小鼠后，在体外和体外均能正常发挥功能。因此，GPIB修饰可能允许冷保存血小板。
Platelet transfusion is a very common lifesaving medical procedure. Not widely known is the fact that platelets, unlike other blood cells, rapidly leave the circulation if refrigerated prior to transfusion. This peculiarity requires blood services to store platelets at room temperature, limiting platelet supplies for clinical needs. Here, we describe the mechanism of this clearance system, a longstanding mystery. Chilling platelets clusters their von Willebrand (vWf) receptors, eliciting recognition of mouse and human platelets by hepatic macrophage complement type 3 (CR3) receptors. CR3-expressing but not CR3-deficient mice exposed to cold rapidly decrease platelet counts. Cooling primes platelets for activation. We propose that platelets are thermosensors, primed at peripheral sites where most injuries occurred throughout evolution. Clearance prevents pathologic thrombosis by primed platelets. Chilled platelets bind vWf and function normally in vitro and ex vivo after transfusion into CR3-deficient mice. Therefore, GPIb modification might permit cold platelet storage.