CJC open · 2025
Relationship Between Vascular Smooth Muscle Cell Phenotype and Degeneration of Elastin in the Aortic Media in Patients With Acute Aortic Dissection.
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Harada Atsushi, Denda Yuya, Koyama Yutaka, Shimodai-Yamada Sayaka, Suzuki Mayumi, van Eys Guillame, Tanaka Masashi, Hao Hiroyuki
Аннотация
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.
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.