弹性纤维蛋白不足及治疗对动脉平滑肌细胞弹性模量的影响。
The effects of elastic fiber protein insufficiency and treatment on the modulus of arterial smooth muscle cells.
作者信息
Gabriela Espinosa M, Gardner William S, Bennett Lisa, Sather Bradley A, Yanagisawa Hiromi, Wagenseil Jessica E
出版信息
J Biomech Eng. 2014 Feb;136(2):021030. doi: 10.1115/1.4026203.
Abstract
Elastic fibers are critical for the mechanical function of the large arteries. Mechanical effects of elastic fiber protein deficiency have been investigated in whole arteries, but not in isolated smooth muscle cells (SMCs). The elastic moduli of SMCs from elastin (Eln-/-) and fibulin-4 (Fbln4-/-) knockout mice were measured using atomic force microscopy. Compared to control SMCs, the modulus of Eln-/- SMCs is reduced by 40%, but is unchanged in Fbln4-/- SMCs. The Eln-/- SMC modulus is rescued by soluble or α elastin treatment. Altered gene expression, specifically of calponin, suggests that SMC phenotypic modulation may be responsible for the modulus changes.
摘要
弹性纤维对大动脉的机械功能至关重要。弹性纤维蛋白缺乏的机械效应已在整个动脉中进行了研究，但尚未在分离的平滑肌细胞（SMC）中进行研究。使用原子力显微镜测量了来自弹性蛋白（Eln-/-）和纤连蛋白-4（Fbln4-/-）基因敲除小鼠的SMC的弹性模量。与对照SMC相比，Eln-/- SMC的模量降低了40%，但Fbln4-/- SMC的模量没有变化。通过可溶性或α弹性蛋白处理可挽救Eln-/- SMC的模量。基因表达的改变，特别是钙调蛋白的改变，表明SMC表型调节可能是模量变化的原因。
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