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BAF60a Deficiency in Vascular Smooth Muscle Cells Prevents Abdominal Aortic Aneurysm Formation by Attenuating Vascular Inflammation

ABSTRACT: BAF60a Deficiency in Vascular Smooth Muscle Cells Prevents Abdominal Aortic Aneurysm Formation by Attenuating Vascular Inflammation

PROVIDER: PRJNA642734 | ENA |

REPOSITORIES: ENA

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RNA-sequencing of abdominal aortic aneurysm (AAA) and control abdominal aorta tissues

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

PRDM16 Deficiency in Vascular Smooth Muscle Cells Aggravates Abdominal Aortic Aneurysm

Project description:Abdominal aortic aneurysm (AAA) is usually asymptomatic until life-threatening complications occur, predominantly involving aortic rupture. Currently, no drug-based treatments are available, primarily due to limited understanding of AAA pathogenesis. The transcriptional regulator PR domain–containing protein 16 (PRDM16) is highly expressed in the aorta, but its functions in the aorta are largely unknown. By RNA-seq analysis, we found that vascular smooth muscle cell–specific (VSMC-specific) Prdm16-knockout (Prdm16SMKO) mice already showed extensive changes in the expression of genes associated with extracellular matrix (ECM) remodeling and inflammation in the abdominal aorta under normal housing conditions without any pathological stimuli. Human AAA lesions displayed lower PRDM16 expression. Periadventitial elastase application to the suprarenal region of the abdominal aorta aggravated AAA formation in Prdm16SMKO mice. During AAA development, VSMCs undergo apoptosis because of both intrinsic and environmental changes, including inflammation and ECM remodeling. Prdm16 deficiency promoted inflammation and apoptosis in VSMCs. A disintegrin and metalloproteinase 12 (ADAM12) is a gelatinase that can degrade various ECMs. We found that ADAM12 is a target of transcriptional repression by PRDM16. Adam12 knockdown reversed VSMC apoptosis induced by Prdm16 deficiency. Our study demonstrated that PRDM16 deficiency in VSMCs promoted ADAM12 expression and aggravates AAA formation, which may provide potential targets for AAA treatment.

2023-06-08 | GSE222440 | GEO

BAF60a Deficiency in Vascular Smooth Muscle Cells Prevents Abdominal Aortic Aneurysm Formation by Attenuating Vascular Inflammation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-21 | GSE153449 | GEO

Circular RNA expression profiles in human abdominal aortic aneurysm

Project description:We have employed circRNA microarray expression profiling as a discovery platform to identify the dysregulated circRNAs in human abdominal aortic aneurysm.

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Single Cell Profiling Identifies the Histone Demethylase, JMJD3, Modulates Macrophage Phenotype in Abdominal Aortic Aneurysm Formation

Project description:Abdominal aortic aneurysm (AAA) is a life-threatening disease characterized by an inflammatory macrophage phenotype that contributes to pathological vascular remodeling. Although the mechanisms regulating macrophage-mediated inflammation during AAA development remain undefined, accumulating evidence suggests that epigenetic alterations play a critical role. Here using single cell RNA-sequencing techniques, we identify that the histone demethylase JMJD3 is elevated in human AAA monocytes/macrophages, resulting in the upregulation of cellular activation and a proinflammatory immune response.

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FAM3A Reshapes Vascular Smooth Muscle Cell Fate Specification in Abdominal Aortic Aneurysm by Regulating KLF4 Ubiquitination

Project description:Vascular smooth muscle cell (VSMC) differentiation reprogramming plays an essential role in abdominal aortic aneurysm (AAA). However, the underlying mechanisms are still indistinct. FAM3A (family with sequence similarity 3, member A) is a newly identified metabolism regulator. We examined FAM3A expression and the downstream pathways affected by FAM3A in AAA, and how FAM3A regulated VSMC differentiation. We found that overexpression or supplement of FAM3A significantly attenuated the progression of AAA, manifested by maintenance of VSMC well-differentiation state and inhibition of VSMC transformation towards macrophage-, chondrocyte-, osteogenic-, mesenchymal-, and fibroblast-like cell subpopulations. Importantly, FAM3A induced a decrease in Krüppel-like factor 4 (KLF4) phosphorylation (Ser254) level, leading to its ubiquitination and a weakened nuclear localization. Our findings identify FAM3A as a novel VSMC fate-shaping regulator in AAA and unveil the underpinning mechanism associated with KLF4 ubiquitination and stability, which could develop new strategies based on FAM3A to restore VSMC homeostasis in AAA.

2023-04-23 | GSE230163 | GEO

Differential gene expression in human abdominal aortic aneurysm and atherosclerosis

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.

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Nicotine administration augments abdominal aortic aneurysm progression in rats

Project description:Inflammation and elastin degradation are key hallmarks in the pathogenesis of abdominal aortic aneurysms (AAA). It has been acknowledged that activation of alpha7 nicotinic acetylcholine receptors (α7nAChRs) attenuates inflammation, termed the cholinergic anti-inflammatory pathway (CAP). Thus, we hypothesized that low-dose nicotine, an α7nAChR agonist, impairs the progression of AAAs in rats by activating the CAP. Male Sprague-Dawley rats underwent surgical AAA induction with intraluminal elastase infusion. We compared vehicle rats with rats treated with nicotine (1.25 mg/kg/day) and the aneurysm progression was monitored by weekly ultrasound images for 28 days. Nicotine significantly promoted AAA progression after 28 days of treatment (p=0.031). Additionally, gelatin zymography demonstrated that nicotine significantly reduced pro-matrix metalloprotease (pro-MMP) 2(p=0.029) and MMP9(p=0.030) activity in aneurysmal tissue. No significant difference was found in elastin content or the score of elastin degradation between the groups. Neither infiltrating neutrophils nor macrophages, nor aneurysmal messenger RNA (mRNA) levels of pro- or anti-inflammatory cytokines differed between the vehicle and nicotine group. Finally, no difference in mRNA levels of markers for antioxidative stress or vascular smooth muscle cells contractile phenotype was observed. However, proteomics analyses of non-aneurysmal abdominal aortas revealed that nicotine decreased proteins in the ontology terms inflammation and reactive oxygen species and in contradiction to augmented AAAs. In conclusion, treatment with the given nicotine dose augmented AAA progression in this rat model.

2023-07-20 | PXD040414 | Pride

The ganglioside GM3 protects against abdominal aortic aneurysm by suppressing ferroptosis in vascular smooth muscle cells

Project description:This project provides insights into the role of ganglioside GM3 in the pathogenesis of abdominal aortic aneurysm (AAA).

2023-09-06 | PXD045177 | iProX