Serial extracellular matrix changes in neointimal lesions of human coronary artery after percutaneous transluminal coronary angioplasty: clinical significance of early tenascin-C expression
Serial extracellular matrix changes in neointimal lesions of human coronary artery after percutaneous transluminal coronary angioplasty: clinical significance of early tenascin-C expression
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DOI：
10.1007/s004280000390
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发表时间：
2001-08-01
期刊：
影响因子：
3.5
通讯作者：
Yoshida, T
中科院分区：
文献类型：
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作者：
Imanaka-Yoshida, K;Matsuura, R;Yoshida, T
细胞外基质（ECM）蛋白的沉积是经皮冠状动脉成形术（PTCA）后再狭窄的主要原因。为了确定人类再狭窄组织中所涉及的ECM的组成和组织，我们对通过定向冠状动脉粥样硬化斑块切除术在PTCA后不同阶段用抗纤连蛋白、腱生蛋白-C、胶原蛋白I和III以及PG-M/多功能蛋白聚糖抗体获得的标本进行形态学和半定量分析。当平滑肌细胞迁移和增殖活跃时，生腱蛋白C沉积在PTCA后1个月内短暂增加。在腱生蛋白-C消失后，PG-M/多功能蛋白聚糖积累增加，并在临床再狭窄进展最活跃的1个月至3个月之间达到峰值。在后期阶段，PG-M/多功能蛋白聚糖被由胶原蛋白I和III组成的更成熟的ECM取代。弹性蛋白的体积比始终保持在低水平。我们的研究结果表明，人类再狭窄病变的基质蛋白在血管成形术后发生了顺序性变化，腱生蛋白-C可能是早期阶段的关键分子。
It has become clear that deposition of extracellular matrix(ECM) proteins is a major cause of human restenosis after percutaneous coronary angioplasty (PTCA). To define the composition and organization of the involved ECM in human restenotic tissue, we morphologically and semiquantitatively analyzed specimens obtained by means of directional coronary atherectomy at various stages after PTCA with anti-fibronectin, tenascin-C, collagens I and III, and PG-M/versican antibodies. Tenascin-C deposition transiently increased within 1 month after PTCA, when smooth muscle cell migration and proliferation was active. Following the disappearance of tenascin-C, PG-M/versican accumulation increased and peaked between 1 month and 3 months when clinical restenosis was most actively progressing. At later stages, the PG-M/versican was replaced by a more mature ECM consisting of collagens I and III. The volume ratio of elastin remained at a low level throughout. Our results demonstrate that the matrix proteins of human restenotic lesions sequentially change after angioplasty and that tenascin-C could be a key molecule in the early stages.