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• W2151779288 abstract "Objective— Even though elastin and fibrillin-1 are the major structural components of elastic fibers, mutations in elastin and fibrillin-1 lead to narrowing of large arteries in supravascular aortic stenosis and dilation of the ascending aorta in Marfan syndrome, respectively. A genetic approach was therefore used here to distinguish the differential contributions of elastin and fibrillin-1 to arterial development and compliance. Methods and Results— Key parameters of cardiovascular function were compared among adult mice haploinsufficient for elastin ( Eln +/− ), fibrillin-1 ( Fbn1 +/− ), or both proteins ( dHet ). Physiological and morphological comparisons correlate elastin haploinsufficiency with increased blood pressure and vessel length and tortuosity in dHet mice, and fibrillin-1 haploinsufficiency with increased aortic diameter in the same mutant animals. Mechanical tests confirm that elastin and fibrillin-1 impart elastic recoil and tensile strength to the aortic wall, respectively. Additional ex vivo analyses demonstrate additive and overlapping contributions of elastin and fibrillin-1 to the material properties of vascular tissues. Lastly, light and electron microscopy evidence implicates fibrillin-1 in the hypertension-promoted remodeling of the elastin-deficient aorta. Conclusions— These results demonstrate that elastin and fibrillin-1 have both differential and complementary roles in arterial wall formation and function, and advance our knowledge of the structural determinants of vascular physiology and disease." @default.
• W2151779288 created "2016-06-24" @default.
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• W2151779288 date "2009-12-01" @default.
• W2151779288 modified "2023-10-16" @default.
• W2151779288 title "Discrete Contributions of Elastic Fiber Components to Arterial Development and Mechanical Compliance" @default.
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• W2151779288 doi "https://doi.org/10.1161/atvbaha.109.193227" @default.
• W2151779288 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2797476" @default.
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