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生物化学和结构证据表明,猪心肌粘附通过心肺旁路破坏结节
C Bianchi1, E G Araujo, K Sato
1Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
Circulation
|September 25, 2001
概括
心肺绕道 (CPB) 导致心血管和细胞中附着结的降解. 这种分子损伤有助于增加血管透性和CPB手术后的心脏功能障碍.
科学领域:
- 心血管科学 心血管科学
- 细胞生物学 细胞生物学
- 手术研究的研究.
背景情况:
- 心肺绕道 (CPB) 与水和心脏功能障碍有关.
- 附着结点对于血管透性和心肌细胞功能至关重要.
研究的目的:
- 为了研究 CPB.猪模型中的附着结交蛋白水平.
- 了解CPB引起的心脏并发症背后的分子机制.
主要方法:
- 猪接受了90分钟的正常热CPB,随后进行了90分钟的再注射.
- 肌肉组织样本被分析到附着结蛋白 (VE-cadherin,β-catenin,gamma-catenin) 使用免疫阻塞和共聚焦显微镜.
- 通过Triton X-100提取评估了附着结的溶解性.
主要成果:
- CPB导致VE-cadherin,β-catenin和gamma-catenin的降解碎片增加.
- 内皮细胞附着结点显示了CPB后降解的迹象.
- 在CPB后,观察到附着结合体复合溶解度的显著增加.
- 聚焦显微镜检测显示,在CPB后的心脏中,细胞-细胞结合被破坏.
结论:
- CPB与内皮细胞和心肌细胞粘附结的降解有关.
- 这种降解代表了一种分子机制,有助于增加血管透性.
- 这些发现表明CPB诱导的心肌细胞功能障碍的途径.
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