AAA pathology in ApoE and CD57BL/6J mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus Musculus
SUBMITTER: 
Yuehong Zheng
PROVIDER: PXD034043 | iProX | Tue May 24 00:00:00 BST 2022
REPOSITORIES: iProX
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Project description:We report the transcriptomic analysis of RNA-seq of abdominal aortas isolated from ApoE-/- and ApoE-/-Nur77-/- mice mice exposed to Ang II to uncover the mechanisms underlying the undefined role of Nur77 in abdominal aortic aneurysm (AAA)
2021-05-21 | GSE174768 | GEO
Project description:Abdominal aortic aneurysm (AAA) is a vascular disease with high incidence at present.There is no effective drug treatment. MicroRNAs(miRNAs) play a regulatory role in the occurrence and development of AAA,and miRNA therapy is a promising treatment for AAA. The purpose of this study was to explore the differential expression of miRNAs in abdominal aorta of ApoE-/- AngII-induced abdominal aortic aneurysm mices. We used miRNA array to analyze miRNA differences in abdominal aorta between mices with ApoE-/- AngII-induced abdominal aortic aneurysm and ApoE-/-.
2025-10-29 | GSE280216 | GEO
Project description:Transcriptional profiling of suprarenal aorta from ApoE-/- mice (12-14 weeks old, C57BL/6J background) treated by subcutaneous pump with angiotensin II or saline for 7d, 14d and 28d. Includes Ang II-treated samples at 7d found to have dissected aneurysms. Goal was to examine gene expression in developing AAA in this model over time. Experiment Overall Design: Two condition experiment, one suprarenal aorta per array. Saline vs. angiotensin II at 3 time points, with inclusion of 3 Ang II-treated dissected. Total 35 arrays: 6 saline 7d, 6 saline 14d, 5 saline 28d, 4 Ang II 7d, 5 Ang II 14d, 6 Ang II 28d, 3 Ang II-dissected 7d.
2009-10-09 | E-GEOD-17901 | biostudies-arrayexpress
Project description:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 µg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis 18 samples analysed, AAA (n=5), no AAA (n=7), saline (n=6). AAA - abdominal aortic aneurysm
2010-06-24 | E-GEOD-12591 | biostudies-arrayexpress
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.
2025-02-14 | GSE285959 | GEO
Project description:Myocardin (Myocd) plays an important role in the maintenance and homeostasis of the vasculature. The loss of Myocd results in vascular smooth muscle cell (VSMC) phenotypic transition and thoracic aortic aneurysms and dissections (TAADs) by downregulating VSMC contractile genes. VSMC phenotypic transition plays a key role in the formation of abdominal aortic aneurysms and dissections (AAADs). However, little is known about the role of Myocd in AAAD. The effect of Myocd on AAA formation was proven in an angiotensin II (Ang II)-induced AAD model. Myocd overexpression or knockdown was achieved by the injection of the corresponding adeno-associated virus serotype 9 (AAV9) through the tail vein. The knockdown of Myocd in C57BL/6J mice treated with angiotensin II promoted the formation of AAAD, as demonstrated by increases in the maximal aortic diameter, vascular inflammation and elastin degradation relative to the control group, while Myocd-overexpressing ApoE-/- mice infused with Ang II were less likely to develop AAAD. Mechanistically, Myocd deficiency significantly repressed VSMC marker gene expression. In addition, qPCR results showed that Myocd knockdown promoted the expression of lncRNAs, which showed increased levels in human AAD tissues. Our results indicated the pivotal role of Myocd in protecting against AAAD formation.
2024-10-25 | GSE180990 | GEO
Project description:Abdominal aortic aneurysm (AAA) is a serious disease with no effective pharmacological therapy. Although inflammation is recognized as a key regulator of AAA, targeting inflammatory pathways once the disease is established does not improve outcomes. Understanding the earliest molecular indicators could clarify precise biological targets and prognostic markers for AAA. Using ApoE-deficient mice, we performed RNA-Seq on suprarenal abdominal aortas (SRAs) from Ang II- and saline-treated mice 24 h after infusion. We further developed a unique model of hyperlipidemic mice in which the expression of the inhibitor of nuclear factor kappa B kinase subunit beta (IKKβ) can be conditionally suppressed in vascular smooth muscle cells (VSMCs). RNA-Seq data revealed early IKKβ-dependent cellular anabolic processes in SRAs, including activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway. Furthermore, deletion of the Ikbkb gene in VSMCs significantly reduced the rate of aneurysm rupture in mice exposed to Ang II. In situ analysis further confirmed that the absence of IKKβ in VSMCs is associated with a reduced inflammatory response and the preservation of their contractile phenotypes. Our results reinforce the crucial role of VSMCs in rapid adaptation, leading to deleterious inflammation-dependent remodeling of the vascular wall, and define a previously unrecognized anabolic role of IKKβ in AAA pathogenesis.
2025-05-28 | GSE265897 | GEO
Project description:Objective: Angiotensin-II (Ang-II) drives pathological vascular wall remodeling in hypertension and abdominal aortic aneurysm (AAA). Previous studies showed that the phosphatase activity of calcineurin (Cn) mediates Ang-II-induced AAA, but the cell type involved in the action of Cn in AAA formation remained unknown. Methods: Smooth muscle cell (SMC)-specific and endothelial cell (EC)-specific Cn-deficient mice (SM-Cn-/- and EC-Cn-/- mice, respectively) were created and assessed for Ang-II-induced AAA formation and hypertension vs controls. Osmotic minipumps were used to administer Ang-II and cyclosporine A (CsA), a pharmaceutical Cn inhibitor. AAA formation and hypertension were monitored by ultrasonography, arterial blood pressure monitoring, and histological analysis. Deep RNA sequencing was used to identify the Ang-II-regulated transcriptome sensitive to Cn deletion or pharmacological inhibition. Arterial and SMC contractility were also assessed. Results: Cn expressed in SMCs, but not ECs, was required for Ang-II-induced AAA. SMC Cn also played an unexpected structural role in the early onset and maintenance of Ang-II-induced hypertension independently of Cn phosphatase activity. Nearly 90% of the genes regulated by Ang-II in the aorta required Cn expression in SMCs. Cn orchestrated, independently of its enzymatic activity, the induction by Ang-II of a gene expression program closely related to SMC contractility and hypertension. Cn deletion in SMCs, but not its pharmacological inhibition, impaired the regulation of arterial contractility. Among the genes whose regulation by Ang-II required Cn expression but not its phosphatase activity, Serpine1 was critical for Ang-II-induced hypertension. Indeed, pharmacological inhibition of PAI-1, the protein encoded by Serpine1, impaired SMCs contractility and regressed hypertension. Conclusions: Whereas the phosphatase activity of Cn mediates Ang-II-induced AAA, a phosphatase-independent action of SMC Cn underlies blood pressure regulation by orchestrating a gene expression program closely related to contractility regulation and hypertension.
2025-04-21 | GSE255061 | GEO
Project description:Dissecting abdominal aortic aneurysm (AAA) is a life-threatening condition characterized by medial layer degeneration of the abdominal aorta. Complex, complicated, and extremely heterogeneous diseases like dissecting AAAs severely limit our ability to understand it. A thorough understanding of cell types and signaling pathways associated with the initiation and progression of dissecting AAA is essential for the development of medical therapy. Single-cell RNA sequencing (scRNA-seq) was performed on the abdominal aortas from ApoE-/- mice at days 28 post-Angiotensin II-induced mouse dissecting AAAs. According to the Angiotensin II-induced dissecting AAA model described in this study, alterations in cellular subpopulations, fractions, and transcriptome profiles are present.
2024-09-19 | GSE239620 | GEO
Project description:Transcriptional profiling of suprarenal aorta from ApoE-/- mice (12-14 weeks old, C57BL/6J background) treated by subcutaneous pump with angiotensin II or saline for 7d, 14d and 28d. Includes Ang II-treated samples at 7d found to have dissected aneurysms. Goal was to examine gene expression in developing AAA in this model over time.
2009-10-01 | GSE17901 | GEO