Texas Heart Institute at St. Luke's Episcopal Hospital, and Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030, USA.
Ann Thorac Surg. 2012 May;93(5):1524-33. doi: 10.1016/j.athoracsur.2012.01.063. Epub 2012 Mar 20.
The hallmark of thoracic aortic aneurysms and dissections (TAAD) is progressive medial degeneration, which can result from excessive tissue destruction and insufficient repair. Although multipotent stem cells (SCs) are important in tissue repair, their role in TAAD is unknown. We sought to determine whether SCs are more abundant in TAAD tissue than in control tissues, and whether SCs within the diseased aortic wall differentiate into functionally relevant cell types.
Using immunohistochemistry, we compared the abundance of STRO-1+ cells, c-kit+ cells, and CD34+ cells in aortic tissue from patients with descending thoracic aortic aneurysms (n=12), patients with chronic descending thoracic aortic dissections (n=18), and age-matched organ donors (n=5). Using double immunofluorescence staining, we evaluated SC differentiation into smooth muscle cells, fibroblasts, and macrophages.
All three cell types were significantly more abundant in the media and adventitia of TAAD tissues than in control tissues. We identified subsets of STRO-1+ cells, c-kit+ cells, and CD34+ cells that also expressed the smooth muscle cell marker SM22-α or fibroblast-specific protein-1, suggesting SC differentiation into smooth muscle cells or fibroblasts. Other STRO-1+ cells expressed the macrophage marker CD68, suggesting differentiation into inflammatory cells.
Stem cells are more abundant in TAAD tissue than in normal aortic tissue. Differentiation of SCs into smooth muscle cells, fibroblasts, and inflammatory cells within the diseased aortic wall suggests that SCs might be involved in both reparative and destructive remodeling processes in TAAD. Understanding the regulation of SC-mediated aortic remodeling will be a critical step toward designing strategies to promote aortic repair and prevent adverse remodeling.
胸主动脉瘤和夹层(TAAD)的标志是进行性中膜退化,这可能是由于组织破坏过多和修复不足所致。虽然多能干细胞(SCs)在组织修复中很重要,但它们在 TAAD 中的作用尚不清楚。我们试图确定在 TAAD 组织中 SC 是否比对照组织更丰富,以及病变主动脉壁内的 SC 是否分化为功能相关的细胞类型。
我们通过免疫组织化学比较了 12 例降胸主动脉瘤患者、18 例慢性降胸主动脉夹层患者和 5 例年龄匹配的器官供体的主动脉组织中 STRO-1+细胞、c-kit+细胞和 CD34+细胞的丰度。使用双重免疫荧光染色,我们评估了 SC 向平滑肌细胞、成纤维细胞和巨噬细胞的分化。
所有三种细胞类型在 TAAD 组织的中膜和外膜中均明显比对照组织丰富。我们鉴定了 STRO-1+细胞、c-kit+细胞和 CD34+细胞的亚群,这些细胞也表达平滑肌细胞标记物 SM22-α 或成纤维细胞特异性蛋白-1,表明 SC 向平滑肌细胞或成纤维细胞分化。其他 STRO-1+细胞表达巨噬细胞标记物 CD68,表明分化为炎症细胞。
SC 在 TAAD 组织中比在正常主动脉组织中更为丰富。SC 在病变主动脉壁内向平滑肌细胞、成纤维细胞和炎症细胞的分化表明,SC 可能参与 TAAD 中的修复和破坏性重塑过程。了解 SC 介导的主动脉重塑的调控将是设计促进主动脉修复和预防不良重塑策略的关键步骤。