Neutrophils and mononuclear cells express vascular endothelial growth factor in acute Kawasaki disease: Its possible role in progression of coronary artery lesions
Neutrophils and mononuclear cells express vascular endothelial growth factor in acute Kawasaki disease: Its possible role in progression of coronary artery lesions
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DOI：
10.1203/00006450-200101000-00017
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发表时间：
2001-01-01
影响因子：
3.6
通讯作者：
Miyawaki, T
中科院分区：
文献类型：
--
作者：
Hamamichi, Y;Ichida, F;Miyawaki, T
川崎（KD）是一种病因不明的全身性血管炎综合征，并发冠状动脉病变（CAL），偶尔导致心脏缺血后遗症。目的探讨血管内皮生长因子（VEGF）是否与川崎病CAL有关。我们通过ELISA测定血清VEGF水平，通过免疫印迹分析测定外周血单个核细胞（PBMC）和中性粒细胞VEGF表达。VEGF水平在急性KD和其他血管炎综合征中显著升高（p < 0.0001）。在10名患有GAL的KD患者中，血清VEGF水平在CAL通常发展时发病后约2周达到最高，并且显著高于20名没有CAL的患者（平均值分别为474和241 pg/mL：p = 0.00015）。在同一时期，免疫印迹分析显示PBMC中VEGF表达最大，与大多数患者的血清VEGF水平相对应，并且在CAL患者中特别显著（p < 0.01）。中性粒细胞仅在急性KD的早期表达VEGF，并且在大多数KD患者中迅速下降，无论是否存在GAL，其表达模式与PBMC明显不同。在其他血管炎综合征患者中，PBMC的VEGF表达也占主导地位，而在正常对照组中仅微弱表达。结果表明VEGF在KD中动态产生，推测反映了其疾病活动性。中性粒细胞来源的VEGF可能在调节早期血管反应中发挥作用，而PBMC来源的VEGF可能有助于后期血管损伤和重塑。
Kawasaki disease (KD) is a syndrome of systemic vasculitis of unknown etiology that is complicated by coronary artery lesions (CAL), leading occasionally to cardiac ischemic sequelae. To examine whether vascular endothelial growth factor (VEGF) is responsible for CAL in KD. we determined serum VEGF levels by ELISA and peripheral blood mononuclear cell (PBMC) and neutrophil VEGF expression by immunoblot analysis. Significantly increased levels of VEGF were demonstrated in acute KD as well as in other vasculitis syndromes (p < 0.0001). In the 10 KD patients with GAL, serum VEGF levels were maximal approximately 2 wk postonset when CAL generally develops and were significantly higher than in 20 patients without CAL (mean, 474 and 241 pg/mL, respectively: p = 0.00015). During the same period, immunoblot analysis revealed maximal VEGF expression in PBMC, corresponding to serum VEGF levels in most patients and being particularly marked in patients with CAL (p < 0.01). Neutrophils expressed VEGF only in the early stage of acute KD and declined rapidly in the majority of KD patients regardless of the presence of GAL, showing a strikingly different expression pattern than that for PBMC. Predominant VEGF expression by PBMC was also demonstrated in patients with other vasculitis syndromes and only faintly in normal controls. The results suggest that VEGF is generated dynamically in KD, presumably reflecting its disease activity. Neutrophil-derived VEGF may play a role in regulating early vascular responses, whereas PBMC-derived VEGF may contribute to later vascular injury and remodeling.