Ang II type 1a receptor in Marfan syndrome

Using Cdh5-Cre and Sm22-Cre transgenes to characterize the impact of disruption of the angiotensin II type 1a receptor (AT1ar) in vascular endothelial and smooth muscle cells, respectively, of wild type (WT) mice compared to fibrillin-1 hypomorphic mice (Fbn1mgR/mgR mice) that replicate early onset progressively severe Marfan syndrome (MFS) with dissecting thoracic aortic aneurysm (TAA). Comparing biological processes identified from transcriptomic analyses of aortic tissue harvested from either WT (at1Rfl) mice or mice with a knockout of AT1ar in either endothelial cells (at1Rcdh5) or smooth muscle cells (at1Rsm22).