急性主动脉夹层患者血管平滑肌细胞表型与主动脉介质弹性蛋白变性的关系

IF 2.5 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

CJC Open Pub Date : 2025-06-01 DOI:10.1016/j.cjco.2025.03.020

Atsushi Harada MD, PhD , Yuya Denda MD, PhD , Yutaka Koyama MD, PhD , Sayaka Shimodai-Yamada MSc , Mayumi Suzuki BSc , Guillame van Eys PhD , Masashi Tanaka MD, PhD , Hiroyuki Hao MD, PhD

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引用次数: 0

摘要

背景：急性主动脉夹层（AAD）是一种危及生命的疾病，在一定比例的患者中没有已知的详细发病机制。虽然已知血管平滑肌细胞（VSMC）的表型调节和细胞外基质（ECM）的变性发生在AAD中，但VSMC表型与ECM变性之间的关系尚不清楚。我们设计了这项研究，以确定夹层主动脉介质中VSMC表型与ECM疾病之间的关系。方法收集24例AAD患者的升主动脉中膜标本，对照17例。使用针对收缩表型标记物平滑肌肌球蛋白重链（SM-MHC）和平滑素以及合成标记物S100A4的抗体进行免疫染色和免疫印迹。结果免疫染色和免疫印迹结果显示，AAD患者中膜SM-MHC和smooththelin的表达水平显著降低，而S100A4的表达水平升高。弹性蛋白（ECM的主要成分）的表达水平在AAD患者中显著降低。收缩标志物（如SM-MHC、smooththelin和elastin）的表达水平之间存在显著的正相关。结论AAD患者VSMCs的表型调节与中膜基质变性可能存在相互作用，可能参与AAD的发病机制。

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Relationship Between Vascular Smooth Muscle Cell Phenotype and Degeneration of Elastin in the Aortic Media in Patients With Acute Aortic Dissection

Background

Acute aortic dissection (AAD) is a life-threatening disease with no known detailed pathogenesis in a certain percentage of patients. Although phenotypic modulation of vascular smooth muscle cells (VSMCs) and degeneration of the extracellular matrix (ECM) are known to occur in AAD, the relationship between the VSMC phenotype and ECM degeneration is unclear. We designed this study to identify the relationship between the VSMC phenotype and ECM disorders in dissected aortic media.

Methods

The tunica media of the ascending aorta was collected from 24 patients with AAD and 17 control autopsy cases. Immunostaining and immunoblotting were performed using antibodies against the contractile phenotypic markers, smooth muscle myosin heavy chain (SM-MHC) and smoothelin, and the synthetic marker, S100A4.

Results

Immunostaining and immunoblotting demonstrated that the expression levels of both SM-MHC and smoothelin were significantly decreased, whereas S100A4 expression levels were elevated, in the tunica media from patients with AAD. The expression level of elastin, a major component of the ECM, was significantly decreased in patients with AAD. There were significant positive correlations between the expression levels of contractile markers, such as SM-MHC, smoothelin, and elastin.

Conclusions

Phenotypic modulation of VSMCs and matrix degeneration in the tunica media of patients with AAD may interact and this phenomenon may contribute to the pathogenesis of AAD.

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