Expression data from mouse aortas

Aortic aneurysm is a life-threatening cardiovascular disorder due to the predisposition for dissection and rupture. Genetic studies have proved the involvement of the transforming growth factor- (TGF-) pathway in aortic aneurysm. Smad4 is the central mediator of canonical TGF- signaling. However, the exact role of Smad4 confined to the smooth muscle cells (SMCs) in the pathogenesis of aortic aneurysm is largely unknown. Furthermore, whether TGF- signaling disruption in SMCs could directly trigger aortic wall inflammation remains poorly investigated. Recently, we revealed a pivotal role of smooth muscle Smad4 signaling in maintaining aortic wall homeostasis and protecting against the development of aortic aneurysm and dissection. To evaluate the underlying mechanism by which Smad4 regulate VSMC functions and affects aneurysm formation and development, Smooth muscle specific Smad4 Knockout mice and the control littermate were sacrificed at 6 weeks old, and their aortic ateries were collected.We combined 3-5 vessels for one sample, and 2 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 2 ug of cRNA were hybridized for 16 hr at 45. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression.

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