Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism
Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism
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DOI：
10.1016/j.jacc.2004.12.075
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发表时间：
2005-05-03
影响因子：
24
通讯作者：
Ahn, YS
中科院分区：
文献类型：
--
作者：
Chirinos, JA;Heresi, GA;Ahn, YS
本研究的目的是确定静脉血栓栓塞症（VTE）患者的血小板、白细胞和内皮细胞活化水平以及细胞相互作用的标志物。静脉血栓栓塞症中内皮细胞、血小板和白细胞之间相互作用的细节还不清楚。我们研究了25例静脉血栓栓塞患者，并比较了25名健康对照者。采用流式细胞术检测：1）内皮细胞微粒（endothelial microparticles，EMP），以CD 31 +/CD 42 b-（EMP 31）或E-选择素（E-selectin，EMP 62 E）标记的血小板微粒（CD 31 +/CD 42 b+）; 3）血小板中P-选择素和白细胞中CD 11b的表面表达; 4）EMP-单核细胞缀合物（E-选择素阳性单核细胞的百分比）;和5）血小板-白细胞缀合物（PLC），表示为CD 41阳性白细胞的百分比。VTE患者的EMP 31显著升高，（2，193 vs. 383计数/μ l; p = 0.003），EMP 62 E（368 vs. 223计数/μ l; p = 0.001）和EMP-单核细胞结合物（3.3% vs. 2.5%; p = 0.002），以及血小板活化增加（P-选择素为35.2对5.0荧光强度单位; p < 0.0001）和白细胞（CD 11b为13.9对7.7 U; p = 0.004）。VTE中PLC也升高（61.7% vs. 39.6%; p = 0.01）。白细胞中CD 11b的表达与PLC密切相关（r = 0.74; p < 0.0001）。内皮细胞、血小板和白细胞的显著活化发生在VTE中，并且VTE或伴随的炎症过程涉及EMP的释放以及EMP-单核细胞缀合物和PLC的形成。这些发现支持了先前的研究，表明EMP的释放及其与单核细胞的结合是血栓形成的关键事件。我们的研究结果也支持PLC的形成调节白细胞活化并参与连接血栓形成与炎症的概念。(c)2005年，美国心脏病学会基金会。
The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). The details of interactions between endothehum, platelets, and leukocytes in VTE are not well understood. We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b-(EMP31) or E-selectin (EMP62E) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. Patients with VTE had marked elevations of EMP31 (2,193 vs. 383 counts/mu l; p = 0.003), EMP62E (368 vs. 223 counts/mu l; p = 0.001), and EMP-monocyte conjugates (3.3% vs. 2.5%; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7% vs. 39.6%; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation. (c) 2005 by the American College of Cardiology Foundation.