Platelet factor 4 localization in carotid atherosclerotic plaques: correlation with clinical parameters
Platelet factor 4 localization in carotid atherosclerotic plaques: correlation with clinical parameters
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DOI：
10.1160/th03-02-0069
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发表时间：
2003-12-01
影响因子：
6.7
通讯作者：
Sachais, BS
中科院分区：
文献类型：
--
作者：
Pitsilos, S;Hunt, J;Sachais, BS
新的证据支持，除了参与血栓性血管闭塞外，血小板在动脉粥样硬化的进展中也发挥了作用。血小板因子4(PF4)是一种由活化的血小板释放的趋化因子，可刺激多种促动脉粥样硬化的过程。因此，我们研究了PF4及其同源蛋白中性粒细胞激活蛋白-2(NAP-2)在代表人类动脉粥样硬化斑块演变的病变中的定位。对132例颈动脉重度狭窄患者和6例尸检标本的颈动脉斑块进行了研究。临床、组织学和免疫组织化学数据采用卡方检验进行分析。PF4定位于管腔和新生血管内皮细胞胞浆、巨噬细胞和斑块钙化区域。巨噬细胞和新生血管内皮细胞中pF4的表达与病变程度呈正相关(p=0.004；p=0.044)。巨噬细胞的PF4染色与症状性动脉粥样硬化性疾病的存在相关(p=0.028)。在早期病变中，PF4在早期病变(I/II级)的巨噬细胞中普遍存在，而NAP-2很少出现。结论：PF4沉积与病变严重程度和症状性动脉粥样硬化之间的相关性表明，持续的血小板激活可能参与了动脉粥样硬化血管病变的演变。这些研究支持在有发生症状性动脉粥样硬化风险的患者中长期使用抗血小板治疗的理论基础。
Emerging evidence supports a role for platelets in the progression of atherosclerosis in addition to an involvement in thrombotic vascular occlusion. Platelet Factor 4 (PF4), a chemokine released by activated platelets, stimulates several pro-atherogenic processes. Therefore, we examined the localization of PF4 and the homologous protein, Neutrophil Activating Protein-2 (NAP-2) in lesions representing the evolution of human atherosclerotic plaques. Carotid plaques from 132 patients with critical carotid stenosis and 6 autopsy specimens were studied. Clinical, histologic and immunohistochemical data were analyzed using a chi(2)-test. PF4 was detected in the cytoplasm of luminal and neovascular endothelium, in macrophages and in regions of plaque calcification. The presence of PF4 in macrophages and neovascular endothelium correlated with lesion grade (p = 0.004; p = 0.044). Staining of macrophages for PF4 correlated with the presence of symptomatic atherosclerotic disease (p = 0.028). In early lesions, PF4 was commonly found in macrophages of early lesions (Grade I/II), whereas NAP-2 was rarely present.In conclusion, correlation between PF4 deposition, lesion severity and symptomatic atherosclerosis suggests that persistent platelet activation may contribute to the evolution of atherosclerotic vascular lesions. These studies support the rationale for the chronic use of anti-platelet therapy in patients at risk for developing symptomatic atherosclerosis.