An intersegmental single-cell profile reveals aortic heterogeneity [AAA]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE191226 | GEO | 2022/05/02
REPOSITORIES: GEO
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Project description:The goals of this study is to compare the differently expressed genes in abdominal aorta tissues of Control and Ang II with or without neferine treatment. The Ang II (n=12) were randomly divided into 2 groups: Ang II , and Ang II + neferine (1 mg/kg/day) groups (n=6 for each group). Control groups (n=5) were set as control. Mouse in Control and Ang II groups were intragastrically with double distilled water (dd H2O); while mice in Ang II + neferine (1 mg/kg/day) group were intragastrically with 1 mg/kg/day of neferine for 6 weeks. Then the abdominal aorta tissues were used to identify differentially expressed genes among different groups.
2023-04-15 | GSE229199 | 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: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:we analyzed proteomics data from ApoE-/- and CD57BL/6J mouse models of Ang II-induced AAA and control mice, which were analyzed abdominal aortic tissues by LC–MS/MS.
2022-05-24 | PXD034043 |
Project description:The goals of this study is to identify the differential expressed genes in abdominal aorta of C57BL/6 mice with or without Angiotensin II (AngII) treatment, and compare the differential expressed genes in the abdominal aorta of Ang II infused C57BL/6 mice after Ethoxysanguinarine (ETH), Baicalin (BAI), Gastrodin (GAS) or valsartan (VAL) treatment. Briefly, the mice (n=30) were randomly divided into 6 groups: control, AngII, AngII + ETH, AngII + BAI, AngII + GAS and AngII + VAL groups (n=5 for each group). Mice in Control and AngII groups were infused with saline and 500 ng/kg/min of AngII respectively, and orally administrated with saline; the mice in AngII + ETH, AngII + BAI and AngII + GAS groups were infused with AngII (500 ng/kg/min) and orally administrated with 5 mg/kg /day of ETH, BAI or GAS daily for total 4 weeks. The mice in AngII + VAL group were infused with AngII (500 ng/kg/min) and orally administrated with 10.4mg/kg /day of VAL. Then the abdominal aortas were used to identify differentially expressed genes among different groups.
2021-05-14 | GSE174386 | GEO
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.
2023-12-07 | GSE183464 | 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:Most blood vessels are surrounded with perivascular adipose tissue (PVAT), which is a unique adipose tissue that plays critical roles in vascular physiology and pathophysiology. PVAT displays regional differences that impact vascular homeostasis. Angiotensin II (Ang II) is the main biological active effector of the renin-angiotensin-aldosterone system (RAAS), which has been extensively studied in the vascular biology. However, the effects of Ang II on PVAT are limited explored and remain to be elucidated. In this study, we systematically investigated the regional heterogeneity of three portions of aortic PVAT, i.e., ascending thoracic aortic PVAT (ATA-PVAT), descending thoracic aortic PVAT (DTA-PVAT), and abdominal aortic PVAT (AA-PVAT), and their responses to 7-day Ang II infusion using RNA sequencing. We found that AA-PVAT is clearly distinguished from both ATA-PVAT and DTA-PVAT, with significantly down-regulated oxidative phosphorylation and up-regulated inflammatory response pathways. Furthermore, AA-PVAT expressed lower levels of brown adipocyte marker genes, such as Ucp1, Cidea, Cox8b, Dio2 and Pgc1α, but expressed higher levels of proinflammatory genes, such as Ccl2, Il1β and Tnfα, and components of the RAAS, including Agt, Ace and Agtr1α. Ang II infusion significantly down-regulated oxidative phosphorylation in all aortic PVAT and significantly up-regulated inflammatory response specifically in ATA-PVAT and DTA-PVAT. Moreover, ATA-PVAT was most responsive to Ang II induced inflammation. We further used a mitoNEET (a.k.a. CDGSH iron sulfur domain 1 protein) transgenic mouse model that exhibited a more brown adipose tissue (BAT)-like phenotype in aortic PVAT, as indicated by elevated expression levels of brown adipocyte marker genes, and confirmed that a more BAT-like phenotype of aortic PVAT could counterbalance Ang II induced inflammatory and oxidative effects.
2025-01-21 | GSE194224 | GEO
Project description:Exercise augments hemodynamic shear to activate mechano-sensitive molecular transducers in the vascular endothelium. Recently, the central nervous system has been reported to mediate neuro-immune interaction in the aortic adventitia (AA). Whether exercise modulates the sympathetic nerve interaction with the immune cells to mitigate aortic stiffness remains unknown. Four weeks of Angiotensin II (Ang II) infusion to C57BL/6 mice increased neural activation to increase the expression of tyrosine hydroxylase (TH) for sympathetic nerve axons and norepinephrine levels along with the colocalization of synapsin and β2-adrenergic receptor (β2-AR) positive macrophages in the AA. This Ang II-mediated sympathetic nerve and macrophage interaction activated fibroblasts to increase vascular fibrosis and arterial pulse wave velocity (PWV). Sympathetic denervation with celiac ganglionectomy or 6-hydroxydopamine treatment abrogated Ang II-mediated TH+, AA thickness, and PWV. scRNAseq analyses of the AA revealed that Ang II increased the circulating monocyte-derived macrophages (Ccr2+CD80) but reduced the resident macrophages (Lyve1+CD163). Gene ontology analysis of differentially expressed genes unveiled that voluntary wheel running (VWR) mitigated Ang II-mediated increase in Ccr2+CD80 macrophages, cytokines-mediated signaling pathways in macrophages, and extracellular matrix deposition in fibroblasts. Macrophage depletion with Ki20227 (colony stimulating factor-1 receptor inhibitor) reduced Ang II-mediated synapsin+ macrophages. Using the Ccr2 knock-in (Ccr2GFP) / knock-out (Ccr2KO) mice, we observed that Ang II-mediated increases in Ccr2+ macrophages were expressed in Ccr2GFP mice but were absent in Ccr2KO mice. Also, Ang II-induced increases in synapsin expression, neighboring Ccr2+ cells, AA thickness, and PWV were reduced in Ccr2KO mice. Both Ki20227 and Ccr2KO reduced the Ang II-mediated increase in TH levels. Furthermore, VWR-mediated reduction in vascular fibrosis and aortic stiffness were mitigated by a β2-AR agonist, terbutaline, indicating β2-AR in neuro-immune modulation. Exercise mitigates Ang II-mediated sympathetic axon interaction with the circulating monocyte-derived macrophages in the AA to attenuate vascular fibrosis and aortic stiffness.
2025-04-11 | GSE291831 | 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