Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components.

Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components.
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定量的而不是定性的组织学区分了动脉瘤和非扩张的升主动脉,并揭示了中层成分的净收益。

DOI:
10.1038/s41598-021-92659-1
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发表时间:
2021-06-23
期刊:
影响因子:
4.6
通讯作者:
Tellides G
Tellides G
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Yousef S;Matsumoto N;Dabe I;Mori M;Landry AB;Lee SR;Kawamura Y;Yang C;Li G;Assi R;Vallabhajosyula P;Geirsson A;Moeckel G;Humphrey JD;Tellides G

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内侧变性是腰椎病的常见组织病理学发现,被认为是扩张的机制。我们研究了中膜变性是否是散发性胸主动脉瘤与非扩张性胸主动脉瘤的特异性。标本由病理学家根据公认的组织病理学标准进行分级,对临床诊断不知情。通过定性(半定量)评估的中膜退变程度与非扩张性动脉瘤相比,对动脉瘤无特异性。相比之下,弹性蛋白量和中膜细胞数的盲法定量评估区分了主动脉瘤和参考标本,尽管结果有明显重叠。具体而言,弹性蛋白的中间部分从稀释而不是蛋白质的损失减少,因为横截面量保持不变,而平滑肌细胞的横截面数量(尽管不是密度)与培养基的扩张成比例增加。此外,弹性层并没有变薄,层间距离并没有减少预期的管腔扩张,这意味着一个净增益的层弹性蛋白和层内细胞或细胞外基质在血管壁重塑。这些发现支持以下概念:(1)中膜退变不一定会诱发主动脉瘤,(2)对改变的机械应力的适应性反应会增加中膜组织,(3)与主动脉扩张相关的壁细胞和细胞外基质的更新(而非损失)更大。
Medial degeneration is a common histopathological finding in aortopathy and is considered a mechanism for dilatation. We investigated if medial degeneration is specific for sporadic thoracic aortic aneurysms versus nondilated aortas. Specimens were graded by pathologists, blinded to the clinical diagnosis, according to consensus histopathological criteria. The extent of medial degeneration by qualitative (semi-quantitative) assessment was not specific for aneurysmal compared to nondilated aortas. In contrast, blinded quantitative assessment of elastin amount and medial cell number distinguished aortic aneurysms and referent specimens, albeit with marked overlap in results. Specifically, the medial fraction of elastin decreased from dilution rather than loss of protein as cross-sectional amount was maintained while the cross-sectional number, though not density, of smooth muscle cells increased in proportion to expansion of the media. Furthermore, elastic lamellae did not thin and interlamellar distance did not diminish as expected for lumen dilatation, implying a net gain of lamellar elastin and intralamellar cells or extracellular matrix during aneurysmal wall remodeling. These findings support the concepts that: (1) medial degeneration need not induce aortic aneurysms, (2) adaptive responses to altered mechanical stresses increase medial tissue, and (3) greater turnover, not loss, of mural cells and extracellular matrix associates with aortic dilatation.
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