Türeyen Kudret, Vemuganti Raghu, Salamat M Shahriar, Dempsey Robert J
Department of Neurological Surgery, University of Wisconsin, Madison, Wisconsin 53792-3232, USA.
Neurosurgery. 2006 May;58(5):971-7; discussion 971-7. doi: 10.1227/01.NEU.0000210246.61817.FE.
Carotid plaque rupture is one of the main causes of stroke by creating cerebral emboli. The biochemical, molecular, and structural factors that promote carotid plaque rupture are not yet understood in detail. We hypothesize that increased microvascular blood flow within a carotid plaque might fissure the plaque, elevate local pressure, and promote plaque rupture. The aim of this study is to determine the role of angiogenesis and angiogenesis-related gene expression in symptomatic carotid plaque.
The present study evaluated the new vessel formation (using hematoxylin-eosin staining and CD34 immunohistochemistry) and angiogenic gene expression (using microarray and real-time polymerase chain reaction analysis) in carotid plaque specimens obtained during endarterectomy from 13 symptomatic stroke patients in comparison with eight asymptomatic patients.
Symptomatic plaques showed significantly higher new vessel density in the fibrous cap (by 347%, P < 0.05) as well as in the plaque proper (by 196%, P < 0.05) compared with the asymptomatic plaques. The fibrous caps of the plaques were threefold thinner in the symptomatic patients when compared with the asymptomatic patients. In symptomatic plaque, gene expression analysis showed increased abundance of 31 transcripts known to promote angiogenesis and cell division compared with plaques of asymptomatic patients.
This study suggests that angiogenic gene expression and the ensuing angiogenesis in the plaques might contribute to their destabilization and resulting symptoms.
颈动脉斑块破裂是形成脑栓塞进而导致中风的主要原因之一。促进颈动脉斑块破裂的生化、分子和结构因素尚未完全明确。我们推测，颈动脉斑块内微血管血流增加可能会使斑块出现裂缝，升高局部压力，从而促进斑块破裂。本研究的目的是确定血管生成及血管生成相关基因表达在有症状颈动脉斑块中的作用。
本研究评估了13例有症状中风患者在接受动脉内膜切除术时获取的颈动脉斑块标本中的新生血管形成情况（采用苏木精-伊红染色和CD34免疫组织化学法）以及血管生成基因表达情况（采用微阵列和实时聚合酶链反应分析），并与8例无症状患者进行了比较。
与无症状斑块相比，有症状斑块的纤维帽处新生血管密度显著更高（增加了347%，P < 0.05），斑块内部也是如此（增加了196%，P < 0.05）。与无症状患者相比，有症状患者斑块的纤维帽薄了两倍。在有症状斑块中，基因表达分析显示，与无症状患者的斑块相比，已知可促进血管生成和细胞分裂的31种转录本丰度增加。
本研究表明，斑块中的血管生成基因表达及随之而来的血管生成可能会导致斑块不稳定并引发相关症状。
