Stromal cell-derived factor 1a facilitates aneurysm remodeling in elastase-induced rabbit saccular aneurysm

Stromal cell-derived factor 1a facilitates aneurysm remodeling in elastase-induced rabbit saccular aneurysm
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基质细胞衍生因子 1α 促进弹性蛋白酶诱导的兔囊状动脉瘤的动脉瘤重塑。

DOI:
10.1016/j.cyto.2017.07.020
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发表时间:
2018-02-01
期刊:
影响因子:
3.8
通讯作者:
Liu, Jian-Min
Liu, Jian-Min
中科院分区:
医学3区
文献类型:
--
作者:
Li, Zi-Fu;Fang, Xing-Gen;Liu, Jian-Min

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目的:炎症在动脉瘤壁重塑中起着至关重要的作用,这可能导致颅内动脉瘤破裂。基质细胞衍生因子Ia(SDF-1 α),一种重要的炎症细胞因子,也与动脉瘤发病机制相关。然而,SDF-1 α表达的特征及其在动脉瘤重塑中的作用在很大程度上仍然未知。在这项研究中,我们的目的是探讨SDF-1 α的表达动态及其与动脉瘤remodeling.Methods的相关性:新西兰白色兔的囊状动脉瘤由猪胰腺弹性蛋白酶诱导。通过数字减影血管造影术测量动脉瘤大小。在术后第1、3、7、14、21和30天评估动脉瘤壁上的内皮样细胞。在几个随访时间点检查了动脉瘤壁和血清中的SDF-1 α水平。粘附分子的表达进行了检查,并在体外进行迁移试验。SDF-1 α刺激后,动员的内皮细胞谱系细胞和它的作用,在动脉瘤壁的再内皮化的囊状动脉瘤兔model.Results:后创建的囊状动脉瘤兔,动脉瘤囊充满急性血栓形成3天内,其次是一个显着的扩大在第14天和成熟的第21天。血清SDF-1 α水平在第1天和第14天以双峰方式增加,而动脉瘤壁中SDF-1 α表达在第14天达到最大值。VE-钙粘蛋白在SDF-1 α刺激后上调,并被SDF-1 α配体阻断剂AMD 3100下调。SDF-1 α可增强内皮祖细胞迁移,AMD 3100可阻断内皮祖细胞迁移。SDF-α的兔囊状动脉瘤的体内管理促进内皮细胞动员到外周血和动脉瘤wall.Conclusions:SDF-1 α的表达水平在外周血和局部动脉瘤壁与动脉瘤重塑过程中的弹性蛋白酶诱导的囊状动脉瘤兔。我们得出结论,SDF-1 α可能通过上调VE-钙粘蛋白表达和动员内皮细胞来促进动脉瘤壁重塑。
Aims: Inflammation plays a crucial role in aneurysm wall remodeling, which could lead to the rupture of intracranial aneurysms. Stromal cell-derived factor la (SDF-1 alpha), a vital inflammation cytokine, is also related to aneurysm pathogenesis. However, the characteristics of SDF-1 alpha expression and its role in aneurysm remodeling remain largely unknown. In this study, we aimed to investigate the expression dynamics of SDF-1 alpha and its correlation with aneurysm remodeling.Methods: Saccular aneurysms were induced by porcine pancreatic elastase in New Zealand White rabbits. Aneurysm size was measured by digital subtraction angiography. Endothelial-like cells on the aneurysm wall were assessed on postoperative days 1, 3, 7, 14, 21, and 30. SDF-1 alpha levels in the aneurysmal wall and serum were examined at several follow-up time points. Adherent molecule expression was examined, and migration assays were performed in vitro. After SDF-1 alpha stimulation, the mobilization of endothelial-lineage cells and its role in the reendothelialization of the aneurysm wall were investigated in a saccular aneurysm rabbit model.Results: After the creation of saccular aneurysms in rabbits, the aneurysm sacs were filled with acute thrombosis within 3 days, followed by a significant enlargement on day 14 and maturation on day 21. Serum SDF-1 alpha levels increased in a bimodal fashion on day 1 and day 14, whereas SDF-1 alpha expression in the aneurysm wall reached its maximum on day 14. VE-cadherin was up-regulated after SDF-1 alpha stimulation and down-regulated by the SDF-1 alpha ligand blocker AMD3100. Endothelial progenitor cell migration was enhanced by SDF-1 alpha and blocked by AMD3100. The in vivo administration of SDF-alpha to rabbits with saccular aneurysms promoted endothelial-lineage cell mobilization into the peripheral blood and reendothelialization of the aneurysm wall.Conclusions: The SDF-1 alpha expression level in the peripheral blood and local aneurysm wall correlated with the aneurysm remodeling process in rabbits with elastase-induced saccular aneurysms. We conclude that SDF-1 alpha may facilitate aneurysm wall remodeling by up-regulating VE-cadherin expression and mobilizing endothelial lineage cells.