慢性大动脉吐中的心肌纤维化:分子和细胞对体积过载的反应
Jeffrey S Borer1, Sharada Truter, Edmund M Herrold
1Division of Cardiovascular Pathophysiology, the Howard Gilman Institute for Valvular Heart Diseases, Department of Anatomy and Cell Biology, Weill Medical College of Cornell University, New York, NY, USA. memontal@med.cornell.edu
Circulation
|April 17, 2002
概括
在大动脉反 (AR) 中,心脏纤维细胞产生异常的细胞外基质 (ECM),特别是纤维素,而不是原. 这种反应主要是由于机械应变,导致心力衰竭.
科学领域:
- 心血管生物学 心血管生物学
- 生物化学 生物化学
- 细胞外矩阵研究研究
背景情况:
- 心肌纤维化是慢性大动脉吐 (AR) 患者的常见并发症.
- 在纤维化中,不成比例的非原细胞外基质 (ECM) 元素在AR中先发并导致心力衰竭.
研究的目的:
- 调查心脏纤维细胞 (CF) 在慢性大动脉反 (AR) 中观察到的改变的ECM组成中的作用.
- 确定与AR相关的机械应变是否是CF这些变化的主要驱动因素.
主要方法:
- 评估了手术诱导慢性AR的子和对照的CF在ECM中的 [3H] - 葡萄糖胺和 [3H] - 的结合.
- 分析了心脏纤维细胞基因表达和特定的ECM蛋白质合成.
- 暴露正常的CF机械应变模仿AR条件来评估初级反应.
主要成果:
- 与对照组相比,来自AR子的CF显示葡萄糖胺结合率增加,纤维素菌素基因表达和合成上调.
- 在AR CF中,proline的整合和原合成 (I型和III型) 保持不变.
- 暴露于机械应变的正常CF表现出增加的葡萄糖胺结合和上调的纤维素,反映了AR发现.
结论:
- 在AR中,心脏纤维细胞产生异常的ECM比例,特别是纤维素,对原蛋白合成的变化很小.
- 由于AR造成的机械应变,至少部分是这些改变的CF反应的主要原因.
- 需要进一步的研究来将这些纤维素变化与AR心力衰竭的发病症联系起来.
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