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In vitro assessment of oxidative stress in the thoracic aorta of a mouse model of Marfan syndrome

Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder, and thoracic aortic aneurysm is a fatal complication. We have shown that MFS compromised aortic vasomotor functions. Endothelial dysfunction (ED) may be caused by oxidative stress where excessive reactive oxygen species interacts and degrades nitric oxide, reducing its bioavailability. Hypothesis: We hypothesized that oxidative stress contributed to ED in the thoracic aorta (TA) of Marfan syndrome. Thoracic aorta from mice (n = 20, 6 months) heterozygous for FBN1 allele (Fbn1C1039G/+, the most common class of MFS) were compared with those from control littermates. In the isometric force measurement, Marfan aorta demonstrated 40% reduction in phenylephrine (PE)‐induced contraction and 30% acetylcholine (ACh)‐mediated relaxation compared with the control. Preincubation with superoxide dismutase (SOD, 150 Units/ml), an enzyme converting superoxide to H2O2, and apocynin (100 μM), an NAD(P)H oxidase inhibitor, suppressed PE response but improved ACh‐relaxation to a greater extent in the Marfan TA. In conclusion, oxidative stress is elevated in the Marfan aorta, and the excess level of superoxide may cause ED. Project was funded by CIHR.