INTRODUCTION: We sought to characterize the gene expression patterns occurring during the development of aneurysms in the native porcine aorta. METHODS: In Yorkshire swine, the infrarenal aorta was balloon dilated and infused with a solution of type I collagenase/pancreatic porcine elastase (16,000 U/1,000 U). Aneurysmal and control aortic samples were obtained at 1 (n = 3), 2 (n = 6), and 4 (n = 5) weeks following aneurysm induction. RNA was isolated, converted to biotin-modified antisense RNA and hybridized to porcine genome arrays. Aneurysmal and control gene intensities were compared using the 2-sample-for-means z-test. P < .01 was considered statistically significant. RESULTS: Extracellular matrix remodeling genes that were upregulated in aneurysmal compared with control tissue included matrix metalloproteinase-1, -2, -3, and -9; MT-MMP; cathepsin-D, -H, -K, and -S; tissue inhibitor of metalloproteinase-1; and collagen I-alpha1 chain (P < .01). Elastin exhibited temporally downregulated gene expression (P < .01). Inflammatory genes that were upregulated included intercellular adhesion molecule-2, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-10, chemokine receptor-4, and tissue plasminogen activator (P < .01). Atherosclerosis and cancer genes that were upregulated included apolipoprotein E, acyl-CoA binding protein, friend leukemia virus integration-1, and E26 transformation-specific sequence (P < .01). CONCLUSION: The porcine model replicates the gene expression patterns that are observed during the development of aneurysms in human studies as well as in rodent models. The porcine model thereby represents a novel method to study the impact of endovascular, cell-based, and other therapeutic interventions on AAA pathophysiology.
INTRODUCTION: We sought to characterize the gene expression patterns occurring during the development of aneurysms in the native porcine aorta. METHODS: In Yorkshire swine, the infrarenal aorta was balloon dilated and infused with a solution of type I collagenase/pancreatic porcine elastase (16,000 U/1,000 U). Aneurysmal and control aortic samples were obtained at 1 (n = 3), 2 (n = 6), and 4 (n = 5) weeks following aneurysm induction. RNA was isolated, converted to biotin-modified antisense RNA and hybridized to porcine genome arrays. Aneurysmal and control gene intensities were compared using the 2-sample-for-means z-test. P < .01 was considered statistically significant. RESULTS: Extracellular matrix remodeling genes that were upregulated in aneurysmal compared with control tissue included matrix metalloproteinase-1, -2, -3, and -9; MT-MMP; cathepsin-D, -H, -K, and -S; tissue inhibitor of metalloproteinase-1; and collagen I-alpha1 chain (P < .01). Elastin exhibited temporally downregulated gene expression (P < .01). Inflammatory genes that were upregulated included intercellular adhesion molecule-2, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-10, chemokine receptor-4, and tissue plasminogen activator (P < .01). Atherosclerosis and cancer genes that were upregulated included apolipoprotein E, acyl-CoA binding protein, friend leukemia virus integration-1, and E26 transformation-specific sequence (P < .01). CONCLUSION: The porcine model replicates the gene expression patterns that are observed during the development of aneurysms in human studies as well as in rodent models. The porcine model thereby represents a novel method to study the impact of endovascular, cell-based, and other therapeutic interventions on AAA pathophysiology.
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