Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome

Abstract

Marfan syndrome, affecting approximately one out of every 5,000 people, is characterized by abnormal bone growth, ectopia lentis, and often-fatal aortic dilation and dissection. The root cause is a faulty extracellular matrix protein, fibrillin-1, which associates with elastin in many tissues. Common carotids from wild-type controls and mice heterozygous for the mgR mutation, the most commonly used mouse model of Marfan syndrome, were studied in a biaxial testing device. Mechanical data in the form of pressure-diameter and force-stretch tests in both the active and passive states were collected, as well data on the functional responses to phenylephrine, carbamylcholine chloride, and sodium nitroprusside. Although little significant difference was found between the heterozygous and wild-type groups in general, the in vivo stretch for both groups was significantly different from previously studied mouse vessels. Although the two groups do not exhibit significant differences, this study comprises a control group for future work with mice homozygous for mgR, which do exhibit Marfan-like symptoms. As treatment of Marfan syndrome improves, more Marfan patients will survive and age, increasing the likelihood that they will develop many of the vascular complications affecting the normal population, including hypertension and atherosclerosis. Therefore, it is imperative to gather biomechanical data from the Marfan vasculature so that clinicians may predict the effects of vascular complications in Marfan patients and develop appropriate methods of treatment.