Thibert V, Bellucci S, Cristofari M, Gluckman E, Legrand C
INSERM U353 Hôpital Saint-Louis, Paris, France.
Br J Haematol. 1995 Nov;91(3):618-24. doi: 10.1111/j.1365-2141.1995.tb05357.x.
The distribution of the major platelet membrane glycoproteins (GP), Ib, IX, IIb-IIIa and IV (or CD36), which play important roles as receptors for adhesive molecules in haemostasis and thrombosis, was studied in 34 patients with myeloproliferative disorders (MPD): 13 had essential thrombocythaemia (ET), 12 had polycythaemia vera (PV) and nine had chronic myelogenous leukaemia (CML). Only occasionally were modifications of the numbers of GPIb or GPIIb-IIIa measured using the binding of specific radiolabelled antibodies to platelets. In contrast, 2-3-fold increases of the total CD36 content and the surface CD36 expression were measured in almost all patients studied, using a radioimmunoassay and the direct binding of the radiolabelled antibody, FA6-152, to the platelet surface, respectively. These results indicate that the abnormality affected both the external and internal CD36 pools. Therefore platelet CD36 may be a useful tool for the diagnosis and the follow-up of MPD patients. Surface CD36 has been proposed as a platelet receptor for thrombospondin, an adhesive glycoprotein that is released from platelets upon activation and promotes aggregate formation. Despite a 2-fold increase of CD36 molecules, resting and thrombin-activated platelets from ET patients expressed the same amount of thrombospondin as normal platelets, suggesting that there is not a direct correlation between the CD36 expression and thrombospondin binding either spontaneously or after activation.
主要血小板膜糖蛋白(GP),即Ib、IX、IIb-IIIa和IV(或CD36),在止血和血栓形成过程中作为黏附分子的受体发挥重要作用。本研究对34例骨髓增殖性疾病(MPD)患者进行了检测,其中13例为原发性血小板增多症(ET),12例为真性红细胞增多症(PV),9例为慢性粒细胞白血病(CML)。仅偶尔使用特异性放射性标记抗体与血小板结合来检测GPIb或GPIIb-IIIa数量的变化。相比之下,几乎所有研究患者的总CD36含量和表面CD36表达分别通过放射免疫分析和放射性标记抗体FA6-152与血小板表面的直接结合检测到增加了2至3倍。这些结果表明该异常影响了CD36的细胞外池和细胞内池。因此,血小板CD36可能是MPD患者诊断和随访的有用工具。表面CD36已被认为是血小板反应蛋白的血小板受体,血小板反应蛋白是一种黏附糖蛋白,在激活时从血小板中释放并促进聚集体形成。尽管CD36分子增加了2倍,但ET患者静息和凝血酶激活的血小板与正常血小板表达相同量的血小板反应蛋白,这表明CD36表达与血小板反应蛋白的自发或激活后结合之间没有直接相关性。