A Method to Quantify Tensile Biaxial Properties of Mouse Aortic Valve Leaflets

A Method to Quantify Tensile Biaxial Properties of Mouse Aortic Valve Leaflets
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DOI:
10.1115/1.4046921
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发表时间:
2020-10-01
影响因子:
1.7
通讯作者:
Hutcheson, Joshua D.
Hutcheson, Joshua D.
中科院分区:
工程技术4区
文献类型:
--
作者:
Chaparro, Daniel;Dargam, Valentina;Hutcheson, Joshua D.

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了解主动脉瓣(AV)力学对于阐明驱动瓣膜疾病表现的机制以及针对这些过程的治疗方式的发展至关重要。转基因小鼠模型已成为评估AV发展和疾病的生物学机制影响的金标准。然而,由于小鼠主动脉瓣小叶(MAVL)的微观尺寸(类似于500 μ m长,45 μ m厚)以及缺乏适当的机械测试模式来评估组织的单轴和双轴拉伸特性,对其拉伸特性知之甚少。我们开发了一种方法,该方法可以通过利用多巴胺作为粘合剂将组织粘附到硅橡胶膜上来评估MAVL组织的双轴拉伸性能。在组织-膜复合材料上施加等轴向拉伸载荷,并在组织表面跟踪工程应变,导致人类和猪组织中AV组织的典型正交各向异性反应。我们的数据表明,在MAVL组织中,周向比径向更硬(n=6, P=0.0006)。这种方法可以在未来的研究中实施,涉及转基因MAVL组织的纵向机械刺激,弥合了流行的小鼠瓣膜疾病模型中细胞生物学机制和瓣膜力学之间的差距。
Understanding aortic valve (AV) mechanics is crucial in elucidating both the mechanisms that drive the manifestation of valvular diseases as well as the development of treatment modalities that target these processes. Genetically modified mouse models have become the gold standard in assessing biological mechanistic influences of AV development and disease. However, very little is known about mouse aortic valve leaflet (MAVL) tensile properties due to their microscopic size (similar to 500 mu m long and 45 mu m thick) and the lack of proper mechanical testing modalities to assess uniaxial and biaxial tensile properties of the tissue. We developed a method in which the biaxial tensile properties of MAVL tissues can be assessed by adhering the tissues to a silicone rubber membrane utilizing dopamine as an adhesive. Applying equiaxial tensile loads on the tissue-membrane composite and tracking the engineering strains on the surface of the tissue resulted in the characteristic orthotropic response of AV tissues seen in human and porcine tissues. Our data suggest that the circumferential direction is stiffer than the radial direction (n=6, P=0.0006) in MAVL tissues. This method can be implemented in future studies involving longitudinal mechanical stimulation of genetically modified MAVL tissues bridging the gap between cellular biological mechanisms and valve mechanics in popular mouse models of valve disease.