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H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

ABSTRACT: H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

PROVIDER: PRJNA953012 | ENA |

REPOSITORIES: ENA

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H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

Project description:H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

| PRJNA953001 | ENA

H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

Project description:To investigate the distribution of H3.3B in VSMC phenotypic transition, we infect VSMCs with shNT or shH3f3b virus.

2024-04-06 | GSE229127 | GEO

H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

Project description:To investigate the function H3f3b in the regulation of VSMC phenotypic transition, we infect VSMCs with shNT or shH3f3b virus.

2024-04-06 | GSE229125 | GEO

Expression data from control, aortic aneurysm, and aortic dissection cells

Project description:Aneurysmatic and dissection cells show a specific alteration of gene expression, which allow a disease specific distinction. We used microarrays to analyse the cellular gene expression of controls, thoracic aortic aneurysm, and aortic dissection.

2022-12-02 | GSE219204 | GEO

The heterogeneity of smooth muscle cells in aortic dissection was determined by single-cell sequencing

Project description:The heterogeneity of smooth muscle cells in aortic dissection was determined by single-cell sequencing

2022-05-30 | GSE203594 | GEO

Expression anaysis of mouse aortic vascular smooth muscle cells

Project description:Analysis of differential gene expression of aortic vascular smooth muscle cells isolated from Tie2floxed:SM22α Cre- (WT) and Tie2floxed:SM22α Cre+ (KO) mice Looking for candidates, that could potentialy be upregulated or downregulated

2017-06-23 | GSE100364 | GEO

Epigenome analysis of ascending aorta from normal, aortic dissection and bicuspid aortic valve patients

Project description:Genome wide DNA methylation profiling of ascending aorta tissue samples from normal, aortic dissection and bicuspid aortic valve patients with aortic dilation. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across more than 450,000 CpGs in ascending aorta samples. Samples included 6 normal donors, 12 patients with aortic dissection and 6 patients with bicuspid aortic valve and dilated aorta.

2019-07-11 | GSE84274 | GEO

miR-145 attenuates phenotypic transformation of aortic vascular smooth muscle cells to prevent aortic dissection.

Project description:BackgroundmiR-145 is closely related to vascular smooth muscle cells (VSMC) phenotype transformation; however, the regulatory mechanisms through which miR-145 regulates the VSMC phenotype transformation under mechanical stretching are unclear. In this study, we evaluated the roles of miR-145 in VSMCs subjected to mechanical stretching in aortic dissection (AD).MethodsThe expression of miR-145 in the aortic vessel wall of model animals and patients with AD was analyzed by quantitative polymerase chain reaction. miR-145-related protein-protein interaction networks and Wikipathways were used to analyze VSMC phenotypic transformation pathways regulated by miR-145. We used gain- and loss-of-function studies to evaluate the effects of miR-145 on VSMC differentiation under mechanical stretch induction and assessed whether Krüppel-like factor 4 (KLF4) was regulated by miR-145 in the aorta under mechanical stretch conditions.ResultsmiR-145 was abundantly expressed in the walls of the normal human aorta, but was significantly downregulated in animal models and the walls of patients with dissection. We found that contractile phenotype-related proteins were downregulated in VSMCs subjected to mechanical stretching, whereas the expression of secreted phenotype-related proteins increased. miR-145 overexpression also downregulated contractile phenotype-related proteins in VSMCs and suppressed upregulation of phenotype-related proteins. Finally, under mechanical stretching, KLF4 expression was significantly increased in VSMCs, and overexpression of miR-145 blocked this effect.ConclusionOur results confirmed that mechanical stretch-induced phenotypic transformation of VSMCs to promote AD via upregulation of KLF4; this mechanism was regulated by miR-145, which directly modulated KLF4 expression and VSMC differentiation.

| S-EPMC8649326 | biostudies-literature

Expression data from aortic dissection patients and the healthy controls

Project description:The mechanisms of acute aortic dissection are not well understood. Transcriptomic strategy has been proven to be an effective way to find the potential mechanisms and also the reliable biomarkers for a specific disease. The whole-genome expression profiling was assayed in a panel of aortic tissues from 4 male acute aortic dissection patients and 4 male healthy controls.

2021-12-12 | GSE190635 | GEO

Aortic smooth muscle cells in bicuspid valve patients

Project description:and with higher incidence if associated to bicuspid aortic valve (BAV) for unknown reasons. TAA is usually diagnosed fortuitously and the lack of effective drug therapy to delay progression and avoid dissection lies in the limited knowledge of pathophysiology. Objectives. We aimed to identify the molecular hallmarks that difference the aortic dilatation associated to bicuspid (BAV) and tricuspid aortic valve (TAV) patients while setting plasma diagnostic molecular panels valve-associated. Methods. Sporadic TAA patients and control subjects (n=91) were classified according to valve type (BAV, TAV). Vascular smooth muscle cells isolated from TAA patients’ aortas were firstly analyzed by mass spectrometry based high-throughput proteomics according to valve type. Extracellularly secreted proteins were secondly analyzed in plasma from TAA patients versus control subjects as diagnostic candidates. Results. Aneurysmal aortas from BAV patients showed a stress phenotype, weakened extracellular matrix interactions, DNA damage and affected protein homeostasis compared to TAV patients. Two plasma marker panels of sporadic TAA valveassociated were identified, showing significant correlation with aortic diameter for C1QTNF5, LAMA2, and SPARC proteins, in BAV patients, and for CP and FAP proteins, in TAV patients. Conclusions. The arterial wall of BAV patients shows a limited capacity to counteract drivers of sporadic TAA while resembling aged arteries.The molecular pathways identified here support the need of differential molecular diagnosis and therapeutic approaches for BAV and TAV patients.

2024-10-17 | PXD043062 | Pride

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