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首页> 外文期刊>Circulation journal >Adipose-derived stem cells stimulate reendothelialization in stented rat abdominal aorta
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Adipose-derived stem cells stimulate reendothelialization in stented rat abdominal aorta

机译：脂肪干细胞刺激带支架的大鼠腹主动脉再内皮化

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Background: Although drug-eluting stents (DES) have been widely used for the treatment of coronary artery disease, they potentially increase the risk of late thrombosis. It is, therefore, desirable to establish a strategy to stimulate reendothelialization. Endothelial injury models have been widely used to analyze the mechanisms of coronary restenosis. However, animal models deployed with coronary stents in the blood vessels are necessary to accurately analyze the mechanisms of coronary restenosis and late thrombosis because persistent inflammation occurs around the coronary stents. Methods and Results: Coronary stents were implanted into rat abdominal aorta and adipose tissue-derived stem cells (ASC) were administered from the adventitial side. Reendothelialization was then visualized by Evans blue staining, and neointimal formation was analyzed histologically. ASC significantly stimulated reendothelialization and inhibited neointimal formation in bare metal stents (BMS)-implanted aorta. In addition, ASC promoted reendothelialization in DES-implanted aorta; however, the effects were weaker than in BMS-implanted aorta. Among the cytokines that ASC produce, adrenomedullin (AM) significantly stimulated reendothelialization and inhibited neointimal formation in BMS-implanted aorta, when an adenovirus expressing AM was administered from the adventitial side. Conclusions: These results suggest that ASC produce several cytokines that stimulate reendothelialization and inhibit neointimal formation in stent-deployed vessels, and that AM could mediate these effects.
机译：背景：尽管药物洗脱支架（DES）已广泛用于治疗冠状动脉疾病，但它们潜在地增加了晚期血栓形成的风险。因此，期望建立一种刺激再内皮化的策略。内皮损伤模型已被广泛用于分析冠状动脉再狭窄的机制。但是，在血管中部署冠状动脉支架的动物模型对于准确分析冠状动脉再狭窄和晚期血栓形成的机制是必要的，因为在冠状动脉支架周围会发生持续的炎症。方法和结果：将冠状动脉支架植入大鼠腹主动脉，并从外膜侧给予源自脂肪组织的干细胞（ASC）。然后通过埃文斯蓝染色观察内皮细胞的内皮化，并通过组织学分析新内膜的形成。 ASC显着刺激了裸金属支架（BMS）植入的主动脉中的内皮再形成并抑制了新内膜的形成。此外，ASC促进了DES植入主动脉的内皮再内皮化。但是，这种作用比BMS植入的主动脉要弱。在ASC产生的细胞因子中，当从外膜侧施用表达AM的腺病毒时，肾上腺髓质素（AM）显着刺激了内皮细胞增生并抑制了BMS植入主动脉中的新内膜形成。结论：这些结果表明，ASC在支架展开的血管中产生多种刺激内皮再形成并抑制新内膜形成的细胞因子，而AM可以介导这些作用。

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