Project description:Angiotensin II (Ang II)-induced abdominal aortic aneurysm model was established in low-density lipoprotein receptor-deficient mice, and the gene expression profiles in abdominal aortic tissues exhibiting varying degrees of severity were analyzed.
Project description:Abdominal aortic aneurysm (AAA) is a permanent segmental dilatation of the abdominal aorta, contributing to a high mortality once rupture. We performed RNA-sequencing analysis of abdominal aorta tissues from 14 participants, including seven patients with AAA and seven control individuals.
Project description:To determine how gene expression is altered in aorta tissue in response to aortic aneurysm disease. Thoracic or abdominal aorta tissue was isolated from patients requiring surgery due to aortic aneurysm or other (control) reason.
Project description:We have employed circRNA microarray expression profiling as a discovery platform to identify the dysregulated circRNAs in human abdominal aortic aneurysm.
Project description:The aim of this study was to assess the relative gene expression in human AAA and AOD. Genome-wide expression analysis of abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) specimens obtained from 20 patients with small AAA (mean maximum aortic diameter=54.3±2.3 mm), 29 patients with large AAA (mean maximum aortic diameter=68.4±14.3 mm), and 9 AOD patients (mean maximum aortic diameter=19.6±2.6 mm). Relative aortic gene expression was compared with that of 10 control aortic specimen of organ donors.
Project description:The aim of this study was to explore the transciptome of the diverse vascular smooth muscle cells subsets from abdominal aortic aneurysm tissues in Gsdme deletion mice.The model was established by exposing the infrarenal aorta to PPE (porcine pancreatic elastase) under pressure to induce aneurysmal degeneration for 4 weeks.we compared the characteristics of SMC subpopulation beteew the WT and KO groupsto reveal the effect of GSDME in the progression of Abdomanl Aortic Aneurysm.
Project description:Thoracic and abdominal aortic aneurysm poses a substantial mortality risk in adults, yet many of its underlying factors remain unidentified. Here, we identify mitochondrial nicotinamide adenine dinucleotide (NAD)⁺ deficiency as a causal factor for the development of aortic aneurysm. Multiomics analysis of 150 surgical aortic specimens indicated impaired NAD+ salvage and mitochondrial transport in human thoracic aortic aneurysm, with expression of the NAD+ transporter SLC25A51 inversely correlating with disease severity and postoperative progression. Genome-wide gene-based association analysis further linked low SLC25A51 expression to risk of aortic aneurysm and dissection. In mouse models, smooth muscle-specific knockout of Nampt, Nmnat1, Nmnat3, Slc25a51, Nadk2 and Aldh18a1, genes involved in NAD+ salvage and transport, induced aortic aneurysm, with Slc25a51 deletion producing the most severe effects. Using these models, we suggest a mechanism that may explain the disease pathogenesis: the production of type III procollagen during aortic medial matrix turnover imposes a high demand for proline, an essential amino acid component of collagen. Deficiency in the mitochondrial NAD⁺ pool, regulated by NAD⁺ salvage and transport, hinders proline biosynthesis in mitochondria, contributing to thoracic and abdominal aortic aneurysm.
Project description:Abdominal aortic aneurysm (AAA) is a common degenerative cardiovascular disease without clear understanding of its pathobiology. To detect AAA associated variants that may affect gene regulation, we generated H3K27ac HiChIP data for aortic smooth muscle cells (AoSMC) and aortic endothelia cells (HAEC), the two cell types most relevant to the AAA disease. We further implemented cell type-specific REs defined from HiChIP experiments, and observed the consistency between the chromatin accessibility of REs and the expression levels of their target genes. Moreover, the cell type-specific REs contributed to detect the AAA most relevant cell type, AoSMC, and locate the important AAA-related TFs, ERG and KLF family.