Purpose: Elastin and collagen (types I and III) are the primary load-bearing elements in aortic tissue. Deficiencies and derangements in elastin and type III collagen have been associated with the development of aneurysmal disease. However, the role of type I collagen is less well defined. The purpose of this study was to define the role of type I collagen in maintaining biomechanical integrity in the thoracic aorta, with a mouse model that produces homotrimeric type I collagen [α1(I)]3, rather than the normally present heterotrimeric [α1(I)]2 α2(I) type I collagen isotype. Methods: Ascending and descending thoracic aortas from homozygous (oim/oim), heterozygous (oim/+), and wildtype (+/+) mice were harvested. Circumferential and longitudinal load-extension curves were used as a means of determining maximum breaking strength (Fmax) and incremental elastic modulus (IEM). Histologic analyses and hydroxyproline assays were performed as a means of determining collagen organization and content. Results: Circumferentially, the ascending and descending aortas of oim/oim mice demonstrated significantly reduced Fmax, with an Fmax of only 60% and 23%, respectively, of wildtype mice aortas. Oim/oim descending aortas demonstrated significantly greater compliance (decreased IEM), and the ascending aortas also exhibited a trend toward increased compliance. Reduced breaking strength was also demonstrated with longitudinal extension of the descending aorta. Conclusion: The presence of homotrimeric type I collagen isotype (absence of α2(I) collagen) significantly weakens the aorta. This study demonstrates the integral role of type I collagen in the biomechanical and functional properties of the aorta and may help to elucidate the role of collagen in the deveopment of aneurysmal aortic disease or dissection.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine