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首页> 外文期刊>American Journal of Physiology >Effects of elastin haploinsufficiency on the mechanical behavior of mouse arteries.
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Effects of elastin haploinsufficiency on the mechanical behavior of mouse arteries.

机译：弹性蛋白单倍体不足对小鼠动脉机械行为的影响。

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摘要

Supravalvular aortic stenosis (SVAS) is associated with decreased elastin and altered arterial mechanics. Mice with a single deletion in the elastin gene (ELN(+/-)) are models for SVAS. Previous studies have shown that elastin haploinsufficiency in these mice causes hypertension, decreased arterial compliance, and changes in arterial wall structure. Despite these differences, ELN(+/-) mice have a normal life span, suggesting that the arteries remodel and adapt to the decreased amount of elastin. To test this hypothesis, we performed in vitro mechanical tests on abdominal aorta, ascending aorta, and left common carotid artery from ELN(+/-) and wild-type (C57BL/6J) mice. We compared the circumferential and longitudinal stress-stretch relationships and residual strains. The circumferential stress-stretch relationship is similar between genotypes and changes <3% with longitudinal stretch at lengths within 10% of the in vivo value. At mean arterial pressure, the circumferential stress in the ascending aortais higher in ELN(+/-) than in wild type. Although arterial pressures are higher, the increased number of elastic lamellae in ELN(+/-) arteries results in similar tension/lamellae compared with wild type. The longitudinal stress-stretch relationship is similar between genotypes for most arteries. Compared with wild type, the in vivo longitudinal stretch is lower in ELN(+/-) abdominal and carotid arteries and the circumferential residual strain is higher in ELN(+/-) ascending aorta. The increased circumferential residual strain brings the transmural strain distribution in ELN(+/-) ascending aorta close to wild-type values. The mechanical behavior of ELN(+/-) arteries is likely due to the reduced elastin content combined with adaptive remodeling during vascular development.
机译：瓣上主动脉瓣狭窄（SVAS）与弹性蛋白减少和动脉力学改变有关。弹性蛋白基因（ELN（+/-））中具有单个删除的小鼠是SVAS的模型。先前的研究表明，这些小鼠的弹性蛋白单倍体不足会导致高血压，动脉顺应性下降和动脉壁结构改变。尽管存在这些差异，ELN（+/-）小鼠的寿命却正常，这表明动脉可以重塑并适应弹性蛋白的减少。为了验证该假设，我们对来自ELN（+/-）和野生型（C57BL / 6J）小鼠的腹主动脉，升主动脉和左颈总动脉进行了体外力学测试。我们比较了周向和纵向应力-拉伸关系和残余应变。基因型之间的周向应力-拉伸关系相似，并且在体内值的10％以内的长度上，纵向拉伸的变化<3％。在平均动脉压下，ELN（+/-）的升主动脉的周向应力高于野生型。尽管动脉压力较高，但与野生型相比，ELN（+/-）动脉中弹性薄片数量的增加导致相似的张力/薄片。大多数动脉的基因型之间的纵向应力-拉伸关系相似。与野生型相比，ELN（+/-）腹主动脉和颈动脉的体内纵向拉伸较低，ELN（+/-）升主动脉的周向残余应变较高。增加的周向残余应变使ELN（+/-）升主动脉中的跨壁应变分布接近于野生型值。 ELN（+/-）动脉的机械行为很可能是由于弹性蛋白含量降低以及在血管发育过程中的适应性重塑所致。

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