The use of transgenic mice is an incredibly powerful tool in understanding the underlying etiology of disease. To understand the usefulness of specific transgenic mice, the systems of interest should be characterized. We have created TGFβ2-deficient mouse fetuses that develop widespread aortic and coronary artery aneurysms . Several studies have pointed to a strong connection between elevated TGFβ signaling and aortic aneurysm . In situ hybridization has shown that Tgfb2 and Tgfb3 are major ligands expressed in the aortic medial wall. Further reduction of TGFβ signaling by combining TGFβ2- and TGFβ3-deficient mice exacerbated cardiovascular aneurysms in TGFβ2/TGFβ3-doubly deficient embryos. In vitro cell culture experiments demonstrated an impaired ability of TGFβ2-deficient mouse embryonic fibroblasts to reorganize collagen. Previous data indicate reduced levels of TGFβ2 leading to a higher susceptibility to aortic aneurysm. We present here the macroscopic biomechanical characterization of the aorta of a transgenic mouse line showing this susceptibility and compare it to wild-type mice. We also present results comparing the microstructure between mouse lines.
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Quantification of the Biomechanical Differences in Wild-Type and Heterozygous TGF Beta2 Knockout Mice
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Keyes, JT, Borowicz, S, Utzinger, U, Azhar, M, & Vande Geest, JP. "Quantification of the Biomechanical Differences in Wild-Type and Heterozygous TGF Beta2 Knockout Mice." Proceedings of the ASME 2010 Summer Bioengineering Conference. ASME 2010 Summer Bioengineering Conference, Parts A and B. Naples, Florida, USA. June 16–19, 2010. pp. 721-722. ASME. https://doi.org/10.1115/SBC2010-19482
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