Gene expression in acute Stanford type A dissection: A comparative microarray study

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Abstract

Background: We compared gene expression profiles in acutely dissected aorta with those in normal control aorta. Materials and methods: Ascending aorta specimen from patients with an acute Stanford A-dissection were taken during surgery and compared with those from normal ascending aorta from multiorgan donors using the BD Atlas™ Human 1.2 Array 1, BD Atlas™ Human Cardiovascular Array and the Affymetrix HG-U133A GeneChip®. For analysis only genes with strong signals of more than 70 percent of the mean signal of all spots on the array were accepted as being expressed. Quantitative real-time polymerase chain reaction (RT-PCR) was used to confirm regulation of expression of a subset of 24 genes known to be involved in aortic structure and function. Results: According to our definition expression profiling of aorta tissue specimens revealed an expression of 19.1% to 23.5% of the genes listed on the arrays. Of those 15.7% to 28.9% were differently expressed in dissected and control aorta specimens. Several genes that encode for extracellular matrix components such as collagen IV α2 and -α5, collagen VI α3, collagen XIV α1, collagen XVIII α1 and elastin were down-regulated in aortic dissection, whereas levels of matrix metalloproteinases-11, -14 and -19 were increased. Some genes coding for cell to cell adhesion, cell to matrix signaling (e.g., polycystin1 and -2), cytoskeleton, as well as several myofibrillar genes (e.g., α-actinin, tropomyosin, gelsolin) were found to be down-regulated. Not surprisingly, some genes associated with chronic inflammation such as interleukin -2, -6 and -8, were up-regulated in dissection. Conclusion: Our results demonstrate the complexity of the dissecting process on a molecular level. Genes coding for the integrity and strength of the aortic wall were down-regulated whereas components of inflammatory response were up-regulated. Altered patterns of gene expression indicate a pre-existing structural failure, which is probably a consequence of insufficient remodeling of the aortic wall resulting in further aortic dissection. © 2006 Weis-Müller et al; licensee BioMed Central Ltd.

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Weis-Müller, B. T., Modlich, O., Drobinskaya, I., Unay, D., Huber, R., Bojar, H., … Sandmann, W. (2006). Gene expression in acute Stanford type A dissection: A comparative microarray study. Journal of Translational Medicine, 4. https://doi.org/10.1186/1479-5876-4-29

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