Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms
Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms
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DOI：
10.1161/circulationaha.104.511717
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发表时间：
2005-08-23
期刊：
影响因子：
37.8
通讯作者：
Tellides, G
中科院分区：
文献类型：
--
作者：
Tang, PCY;Coady, MA;Tellides, G
背景-进行性中膜变性和萎缩被认为是老年人胸升主动脉瘤的一个原因。腹主动脉瘤中存在大量的血管平滑肌细胞凋亡。我们调查是否发生在原发性胸升主动脉瘤的VSMCs的损失内侧萎缩。方法和结果-28 nonacuptamous胸升主动脉瘤和29个胸升主动脉瘤的形态定量分析进行了直接测量其血管层的厚度和间接计算其血管车厢的面积。在结构、蛋白质和转录水平评估培养基的细胞和基质组成。尽管继发于血管扩张的中膜变薄，但动脉瘤的内侧区域总体增加。VSMC密度保持不变，表明中膜质量增加导致细胞增生。基质蛋白的表达减少，尽管这些分子持续合成，这与基质降解增加的证据有关。的重塑和扩大的媒体是最明显的nonaerosymal动脉瘤与较小的动脉瘤之间的比较，并没有进一步发展在较大的aneurysms.Conclusions -腔扩大在胸主动脉瘤和腹主动脉瘤的机制显着不同方面的VSMC的生存和萎缩的媒体，但共同的病理生理学涉及退化的矩阵。胸升主动脉瘤中膜的增生性细胞重塑可能是最初的适应性反应，以尽量减少血管扩张引起的壁应力增加。
Background - Progressive medial degeneration and atrophy is thought to be a cause of ascending thoracic aortic aneurysms in the elderly. Extensive apoptosis of vascular smooth muscle cells (VSMCs) has been demonstrated in the media of abdominal aortic aneurysms. We investigated whether medial atrophy from loss of VSMCs occurs in primary ascending thoracic aortic aneurysms.Methods and Results - Morphometric analysis of 28 nonaneurysmal ascending thoracic aortas and 29 ascending thoracic aortic aneurysms was performed by directly measuring the thickness of their vascular layers and by indirectly calculating the area of their vascular compartments. The cellular and matrix composition of the media was assessed at the structural, protein, and transcript levels. Despite thinning of the media secondary to vascular dilatation, there was an overall increase in the medial area of aneurysms. VSMC density was preserved, implying cellular hyperplasia as a result of the increased medial mass. There was decreased expression of matrix proteins, despite sustained synthesis of these molecules, which was associated with evidence of increased matrix degradation. The remodeling and expansion of the media was most evident in comparisons between nonaneurysmal aortas versus smaller aneurysms and did not evolve further in larger aneurysms.Conclusions - The mechanisms for luminal enlargement in thoracic and abdominal aortic aneurysms differ significantly with regard to the survival of VSMCs and atrophy of the media but share common pathophysiology involving degeneration of the matrix. Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms may be an initial adaptive response to minimize increased wall stress resulting from vascular dilatation.