Inhibiting YAP1 reduced abdominal aortic aneurysm formation by suppressing adventitial fibroblast phenotype transformation and migration

Cuiping Xie, Yanting Hu, Zhehui Yin
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Abstract

The adventitial fibroblast (AF) is the most abundant cell in the vascular adventitia, a few studies had confirmed that AF contributed to abdominal aortic aneurysm (AAA) development; YAP1 involved in several vascular diseases by promoting AF transformed to myofibroblast, the role of YAP1 in AAA is not clear yet. This study aims to determine whether YAP1 play a role in AAA process by regulating AF function. We found the expression of YAP1was significantly increased in aneurysm tissues of AAA patients compared to normal adjacent vascular tissues and mainly in adventitia. YAP1 also upregulated in elastase-induced and CaCl2-induced mice AAA model. Suppressed YAP1 function with YAP1 inhibitor-Verteporfin declined AAA incident rate remarkably in mice, and the collagen deposition in the adventitia was alleviated obviously. Afterwards, we studied the effect of YAP1 on the function of AF, Verteporfin was used to block YAP1 in vitro, the process of AF transforming to myofibroblast and migration were almost completely eliminated after inhibiting YAP1 expression. This study demonstrated that YAP1 may play a key role in AAA development, inhibiting YAP1 significantly reduced AAA formation through suppressed the process of AF transformed to myofibroblast and migration.

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抑制 YAP1 可抑制临近纤维母细胞的表型转化和迁移,从而减少腹主动脉瘤的形成。
血管内膜成纤维细胞(AF)是血管内膜最丰富的细胞,一些研究证实AF是腹主动脉瘤(AAA)发生的诱因之一;YAP1通过促进AF向肌成纤维细胞转化而参与多种血管疾病,但YAP1在AAA中的作用尚不明确。本研究旨在确定 YAP1 是否通过调控 AF 功能在 AAA 过程中发挥作用。我们发现,与正常邻近血管组织相比,YAP1在AAA患者动脉瘤组织中的表达明显增加,且主要在动脉瘤的血管内膜。在弹性蛋白酶诱导和 CaCl2 诱导的小鼠 AAA 模型中,YAP1 也上调。用YAP1抑制剂-Verteporfin抑制YAP1功能,可显著降低小鼠AAA的发病率,并明显减轻血管内膜的胶原沉积。随后,我们研究了YAP1对AF功能的影响,在体外用Verteporfin阻断YAP1,抑制YAP1表达后,AF向肌成纤维细胞转化和迁移的过程几乎完全消失。这项研究表明,YAP1可能在AAA的发生发展中起着关键作用,抑制YAP1可通过抑制AF向肌成纤维细胞转化和迁移的过程,显著减少AAA的形成。
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期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
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