Humoral and cellular factors responsible for coronary collateral formation
Humoral and cellular factors responsible for coronary collateral formation
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DOI：
10.1016/j.amjcard.2006.05.046
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发表时间：
2006-11-01
影响因子：
2.8
通讯作者：
Simons, Michael
中科院分区：
文献类型：
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作者：
Sherman, Jonathan A.;Hall, Amy;Simons, Michael
临床观察表明，尽管冠状动脉阻塞程度相似，但冠状动脉疾病（CAD）患者的侧枝循环形成存在明显的异质性。冠状动脉侧支循环的发育有助于保护心肌免受缺血性损伤，但对侧支循环形成的影响因素却知之甚少。为了更好地了解侧支动脉形成的生化和细胞机制，我们对 101 名经血管造影评估 CAD 且侧支循环广泛发育（评分 2，n = 33）或缺失（评分 0，n = 68）的患者的单核细胞功能以及促血管生成因子和抗血管生成因子的循环水平进行了测量。与评分为 0 的患者相比，评分为 2 的患者年龄稍大，并且患有更严重的 CAD。评分 2 组也更有可能有既往心肌梗塞或冠状动脉搭桥术以及 CAD 家族史。同时，血管内皮生长因子-A(165)、血小板源性生长因子-β、成纤维细胞生长因子-2、成纤维细胞生长因子-4、肝细胞生长因子、肿瘤坏死因子-α、白细胞介素-1β、内皮抑素、基质金属蛋白酶-9、 前基质金属蛋白酶-1 和 CD40 配体。从侧支循环评分为 2 和 0 的患者中分离出的单核细胞在迁移测定中没有显示差异。然而，评分为 0 的患者的单核细胞对纤维蛋白原和胶原蛋白的粘附显着较高（分别为 p = 0.05 和 0.04）。总之，这些数据表明，冠状动脉侧支形成的程度并不是由本研究中评估的促血管生成因子或抗血管生成因子的系统可测量水平的差异决定的。相反，细胞特性，例如细胞粘附或患者之间的遗传差异可能是附带发育的驱动力。 (c) 2006 Elsevier Inc. 保留所有权利。
Clinical observations suggest that patients with coronary artery disease (CAD) display a marked heterogenerty in collateral formation despite similar degrees of coronary obstruction. The development of coronary collaterals helps protect the myocardium from ischemic damage, yet the factors responsible for collateral formation are poorly understood. To better understand the biochemical and cellular mechanisms of collateral artery formation, monocyte function and circulating levels of pro- and antiangiogenic factors were measured in 101 patients with angiographically assessed CAD and extensively developed (score 2, n = 33) or absent (score 0, n = 68) collateral circulations. Compared with patients with score 0, those with score 2 were slightly older and had more advanced CAD. The score 2 group, was also more likely to have had a previous myocardial infarction or coronary artery bypass grafting and a family history of CAD. At the same time, there were no significant differences between groups with regard to circulating levels of vascular endothelial growth factor-A(165), platelet-derived growth factor-beta beta, fibroblast growth factor-2, fibroblast growth factor-4, hepatocyte growth factor, tumor necrosis factor-alpha, interleukin-1 beta, endostatin, matrix metalloproteinase-9, promatrix metalloproteinase-1, and CD40 ligand. Monocytes isolated from patients with score 2 and 0 collateral circulations demonstrated no differences in migration assays. However, adhesion to fibrinogen and collagen was significantly higher for monocytes from patients with score 0 (p = 0.05 and 0.04, respectively). In conclusion, these data suggest that the degree of coronary collateral formation is not determined by differences in systemically measurable levels of pro- or antiangiogenic factors assessed in this study. Rather, cellular properties, such as cell adhesion, or genetic differences between patients may be the driving force for collateral development. (c) 2006 Elsevier Inc. All rights reserved.