Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1004189 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25597336.fastq.gz | Fastqsanger.gz | |||
| SRR25597337.fastq.gz | Fastqsanger.gz | |||
| SRR25597338.fastq.gz | Fastqsanger.gz | |||
| SRR25597339.fastq.gz | Fastqsanger.gz | |||
| SRR25597340.fastq.gz | Fastqsanger.gz |
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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: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:Vascular smooth muscle cell (VSMC) phenotypic switching is widely recognized as a key mechanism responsible for the pathogenesis of several aortic diseases such as aortic aneurysm. Cellular communication network factor 2 (CCN2), often upregulated in human pathologies and animal disease models, exerts a myriad of context-dependent biological functions. However, current understanding of the role of SMC-CCN2 in SMC phenotypic switching and its function in the pathology of abdominal aortic aneurysm (AAA) is lacking. Here we report the effect of SMC-restricted CCN2 deficiency of hypercholesterolemic mice on gene expression in infrarenal aorta with or without angiotensin II (Ang II)-infusion.
2023-03-02 | GSE221399 | GEO
Project description:Abdominal aortic aneurysm (AAA) and the attendant catastrophic event of rupture remain a leading cause of death. During AAA, VSMCs lost contractile-related phenotype, with reduced levels of actin alpha 2, smooth muscle (ACTA2), transgelin (TAGLN) and calponin 1 (CNN1)) , and obtain ability to secrete matrix metalloproteinases to degrade the extracellular matrix and weaken the arterial wall, which potentiate the rupture of the aneurysm. Angiotensin 2 (Ang II) can induce phenotype transition of VSMCs，while the underlying mechanism remains elusive. Here we found Ang II treatment could reduce expression of R-Ras2, thus reducing the phosphorylation and nuclear translocation of TFII-I, as a result, the gene expression of ACTA2, TAGLN and CNN1 were inhibited and VSMCs lost the contractile phenotype.
2025-06-29 | GSE291516 | 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: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:Objective: A cardinal feature of Marfan syndrome is thoracic aortic aneurysm. The contribution of the renin-angiotensin system via AT1aR (Ang II [angiotensin II] receptor type 1a) to thoracic aortic aneurysm progression remains controversial because the beneficial effects of angiotensin receptor blockers have been ascribed to off-target effects. This study used genetic and pharmacological modes of attenuating angiotensin receptor and ligand, respectively, to determine their roles on thoracic aortic aneurysm in mice with fibrillin-1 haploinsufficiency (Fbn1C1041G/+). Approach and Results: Thoracic aortic aneurysm in Fbn1C1041G/+ mice was found to be strikingly sexual dimorphic. Males displayed aortic dilation over 12 months while aortic dilation in Fbn1C1041G/+ females did not differ significantly from wild-type mice. To determine the role of AT1aR, Fbn1C1041G/+ mice that were either +/+ or −/− for AT1aR were generated. AT1aR deletion reduced expansion of ascending aorta and aortic root diameter from 1 to 12 months of age in males. Medial thickening and elastin fragmentation were attenuated. An antisense oligonucleotide against angiotensinogen was administered to male Fbn1C1041G/+ mice to determine the effects of Ang II depletion. Antisense oligonucleotide against angiotensinogen administration attenuated dilation of the ascending aorta and aortic root and reduced extracellular remodeling. Aortic transcriptome analyses identified potential targets by which inhibition of the renin-angiotensin system reduced aortic dilation in Fbn1C1041G/+ mice. Conclusions: Deletion of AT1aR or inhibition of Ang II production exerted similar effects in attenuating pathologies in the proximal thoracic aorta of male Fbn1C1041G/+ mice. Inhibition of the renin-angiotensin system attenuated dysregulation of genes within the aorta related to pathology of Fbn1C1041G/+ mice.
2025-07-07 | GSE301765 | GEO
Project description:According to the new scRNA-seq data after batch correction, we obtained 22, 975 cells totally isolated from aortic tissues of three groups including healthy abdominal aorta group (AA group), Ang II+ DMSO group (D_A group) and Ang II+ Inhibitor group (IN_A group)
2022-05-02 | GSE191226 | GEO
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:We analyzed differentially expressed genes in aortas from Apoe-/- mice that received Apoe-/- bone marrow or Apoe-/-Sept2C111A bone marrow and were infused with Ang II for 28 days to explore the mechanisms of macrophage SNO-Septin2 in aortic aneurysm development.
2024-11-03 | GSE246974 | GEO