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The Effects of Elastic Fiber Protein Insufficiency and Treatment on the Modulus of Arterial Smooth Muscle Cells

机译:弹性纤维蛋白不足和治疗对动脉平滑肌细胞模量的影响

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摘要

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.
机译:弹性纤维对于大动脉的机械功能至关重要。弹性纤维蛋白缺乏的机械作用已在整个动脉中进行了研究,但在孤立的平滑肌细胞(SMCs)中尚未进行研究。使用原子力显微镜测量弹性蛋白(Eln-/-)和fibulin-4(Fbln4-/-)敲除小鼠的SMCs的弹性模量。与对照SMC相比,Ern-/-SMC的模量降低了40%,但在Fbln4-/-SMC中没有变化。 Eln //-SMC模量通过可溶性或弹性蛋白处理得以挽救。改变基因的表达,特别是钙蛋白的表达,表明SMC表型调节可能是导致模量变化的原因。

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