Modelling Atherosclerotic Plaque Cap Mechanics: Microcalcifications Reduce Mechanical Properties in Mesenchymal Stromal Cell-Based Model.

IF 2.6 3区 生物学 Q3 MATERIALS SCIENCE, BIOMATERIALS
Imke L Jansen, Deniz Şahin, Frank J H Gijsen, Eric Farrell, Kim van der Heiden
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引用次数: 0

Abstract

Rupture of atherosclerotic plaque caps is the cause of many disabling or lethal cardiovascular events, such as stroke and myocardial infarction. Microcalcifications (<50 µm) have been shown, in computational models, to affect the biomechanical stability of the cap. The current study aims to develop a tissue-engineered model of the atherosclerotic fibrous cap with microcalcifications produced by mesenchymal stromal cells (MSCs). Human MSCs are seeded in fibrin gels and cultured for 2 weeks in medium supplemented with TGF-β1 to induce smooth muscle cell differentiation and collagenous matrix formation. Afterward, mineralizing medium stimulates microcalcification formation for an additional 4 weeks. Tissue-engineered structures are imaged after culture with second harmonic generation microscopy with a hydroxyapatite probe, showing collagenous matrix with microcalcifications. Mechanical characterization shows the effect of microcalcifications on global tissue mechanics, as the ultimate stress at rupture of the tissue is significantly lower compared to control tissues. The amount of calcification, determined by histological analysis, is correlated to the decrease in ultimate tensile stress, with a higher amount of microcalcification resulting in weakened mechanical properties. The developed tissue-engineered plaque cap model with biologically formed collagenous matrix and microcalcifications offers valuable insight into the impact of microcalcifications on biomechanical stability.

模拟动脉粥样硬化斑块帽力学:微钙化降低间充质间质细胞模型的力学特性。
动脉粥样硬化斑块帽破裂是许多致残或致命心血管事件的原因,如中风和心肌梗死。微钙化物质(
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来源期刊
Advanced biology
Advanced biology Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
6.60
自引率
0.00%
发文量
130
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