LncRNA Expression Profile of Human Thoracic Aortic Dissection by High-Throughput Sequencing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA421670 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6362802_1.fastq.gz | Fastqsanger.gz | |||
| SRR6362802_2.fastq.gz | Fastqsanger.gz | |||
| SRR6362803_1.fastq.gz | Fastqsanger.gz | |||
| SRR6362803_2.fastq.gz | Fastqsanger.gz | |||
| SRR6362804_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:In this study, the long non-coding RNA (lncRNA) expression profile in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated. Human TAD (n=3) and normal aortic tissues (NA) (n=3) were examined by high-throughput sequencing. Bioinformatics analyses were performed to predict the roles of aberrantly expressed lncRNAs. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to validate the results. A total of 269 lncRNAs (159 up-regulated and 110 down-regulated) and 2, 255 mRNAs (1 294 up-regulated and 961 down-regulated) were aberrantly expressed in human TAD (fold-change>1.5, P<0.05). QRT-PCR results of five dysregulated genes were consistent with HTS data. A lncRNA-mRNA coexpression analysis showed positive correlations between the up-regulated lncRNA (ENSG00000269936) and its adjacent up-regulated mRNA (MAP2K6, R=0.940, P<0.01), and between the down-regulated lncRNA_1421 and its down-regulated mRNAs (FBLN5, R=0.950, P<0.01; ACTA2, R=0.96, P<0.01; TIMP3, R=0.96, P<0.05). The lncRNA-miRNA-mRNA network indicated that the up-regulated lncRNA XIST and p21 had similar sequences targeted by has-miR-17-5p. The results of luciferase assay and fluorescence immuno-cytochemistry were consistent with that. And qRT-PCR results showed that lncRNA XIST and p21 were expressed at a higher level and has-miR-17-5p was expressed at a lower level in TAD than in NA. The predicted binding motifs of three up-regulated lncRNAs (ENSG00000248508, ENSG00000226530, and EG00000259719) were correlated with up-regulated RUNX1 (R=0.982, P<0.001; R=0.967, P<0.01; R=0.960, P<0.01, respectively). Our study revealed a set of dysregulated lncRNAs and predicted their multiple potential functions in human TAD. These findings suggest that lncRNAs are novel potential therapeutic targets for human TAD.
2020-11-30 | GSE107844 | GEO
Project description:Thoracic aortic dissection (TAD) is associated with a high mortality rate. Despite the existence of different mouse models for TAD, the underlying disease mechanisms remain elusive. Treatment options are limited and mainly consist of surgical repair at critical diameters as current pharmacological interventions are unable to stop disease progression. In humans, loss of function (LOF) of SMAD3 and SMAD6 impair vascular homeostasis, increasing the risk for TAD. We developed a zebrafish model for thoracic aortic dissection/rupture by targeting both ohnologs of smad3 and smad6. We discovered an increased diameter of the ventral aorta in smad3a-/-;smad3b-/- double knockout zebrafish larvae, while smad6a-/-;smad6b-/- double knockout zebrafish have a reduced diameter associated with early mortality. Surprisingly, the smad3a-/-;smad3b-/-;smad6a-/-;smad6b-/- quadruple knockout (qKO) zebrafish model is viable and survives to adulthood, although exposure to stress leads to sudden death. Histological analysis of the adult ventral aorta showed medial elastolysis and aortic dissections and ruptures at sites exposed to high hemodynamic stress. RNA-sequencing of qKO larvae indicated a profile of reduced negative regulation of proteolysis and upregulation of melanogenesis, a previously unaddressed pathway in this pathology. We confirmed that pharmacological modulation of tyrosinase has an effect on aortic morphology. Our study shows that dysregulation of SMAD3/6-dependent signaling has an important impact on thoracic aortic homeostasis, and that using the qKO zebrafish model, thus far the only known model of aortic dissection and rupture in this species, can identify novel pathophysiological pathways leading to TAD.
2025-01-13 | GSE249792 | GEO
Project description:To assess the circular RNAs (circRNAs) expression profile and explore the potential functions in human thoracic aortic dissection (TAD).The differentially expressed circRNAs profiles of the aortic segments between human type A TAD patients (n=3) and age-matched normal donors (NA; n=3) were analyzed using the Arraystar human circRNAs microarray. Quantitative real-time PCR was used to validate the expression pattern of circRNAs, parental genes, and hsa-miR-320a; Western blotting confirmed MMP9 expression with additional samples. Bioinformatic tools including network analysis, Gene ontology, and KEGG pathway analysis were utilized.
2020-04-12 | GSE97745 | GEO
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
Project description:Descending thoracic aortic aneurysms and dissections can go undetected until severe and catastrophic, and few clinical indices exist to screen for aneurysms or predict their risk of dissection or rupture. This study generated a plasma proteomic dataset from 150 patients with descending thoracic aortic disease and 52 controls to identify proteomic signatures capable of differentiating descending thoracic aortic disease from non-disease controls, as well as between cases with aneurysm versus descending ‘type B’ dissection. Of the 1,468 peptides and 195 proteins quantified across all samples, 853 peptides and 99 proteins were quantitatively different between disease and control patients (BH adjusted p-value < 0.01 from t-tests). Supervised machine learning (ML) methods were used to classify disease from control and aneurysm from descending dissection cases. The highest precision-recall area under the curve (PR AUC) was achieved on the held-out test set using significantly different proteins between disease and control patients (PR AUC 0.99), followed by input of significant peptides (PR AUC 0.96). Despite no statistically significant proteins between aneurysm and dissection cases, use of all proteins was able to modestly classify between the two disease states (PR AUC 0.77). To overcome correlation in the proteins and enable biological pathway analysis, a disease versus control classifier was optimized using only seven unique protein clusters, which achieved comparable performance to models trained on all/significant proteins (accuracy 0.88, F1-score 0.78, PR AUC 0.90). Model interpretation with permutation importance revealed that proteins in the most important clusters for differentiating disease and control function in coagulation, protein-lipid complex remodeling, and acute inflammatory response.
2024-06-16 | PXD041337 | Pride
Project description:Aortic dissection (AD) is a cardiovascular emergency resulted from blood flows into vessel wall, with high mortality in early stage. Due to the vital pathological mechanism for AD occurrence has not been clarified, and no effective ways to prevent and diagnose AD’s process. In this study, we determine the lncRNA expression profile in aortic dissection group and control group. The key lncRNAs were screen out by using microarray analysis in defferent group.
2021-09-15 | GSE183997 | GEO
Project description:Early mechanisms of aortic failure in a zebrafish model for thoracic aortic dissection and rupture
| PRJNA1050594 | ENA
Project description:Adverse aortic remodeling increases the risk of aorta-related adverse events (AAEs) after thoracic endovascular aortic repair (TEVAR) and affects the overall prognosis of aortic dissection (AD). It is imperative to delve into the exploration of prognostic indicators to We performed single-cell transcriptomic and proteomic profiling of aortic lesions and peripheral blood samples, respectively, from patients with AD and healthy subjects. We then integrated single-cell RNA to identify phenotype-relevant subpopulations.
2024-11-01 | GSE254132 | GEO
Project description:Thoracic and abdominal aortic aneurysm poses a substantial mortality risk in adults, yet many of its underlying factors remain unidentified. Here, we identify mitochondrial nicotinamide adenine dinucleotide (NAD)⁺ deficiency as a causal factor for the development of aortic aneurysm. Multiomics analysis of 150 surgical aortic specimens indicated impaired NAD+ salvage and mitochondrial transport in human thoracic aortic aneurysm, with expression of the NAD+ transporter SLC25A51 inversely correlating with disease severity and postoperative progression. Genome-wide gene-based association analysis further linked low SLC25A51 expression to risk of aortic aneurysm and dissection. In mouse models, smooth muscle-specific knockout of Nampt, Nmnat1, Nmnat3, Slc25a51, Nadk2 and Aldh18a1, genes involved in NAD+ salvage and transport, induced aortic aneurysm, with Slc25a51 deletion producing the most severe effects. Using these models, we suggest a mechanism that may explain the disease pathogenesis: the production of type III procollagen during aortic medial matrix turnover imposes a high demand for proline, an essential amino acid component of collagen. Deficiency in the mitochondrial NAD⁺ pool, regulated by NAD⁺ salvage and transport, hinders proline biosynthesis in mitochondria, contributing to thoracic and abdominal aortic aneurysm.
2024-11-19 | GSE235161 | GEO
Project description:MiRNA analysis in Thoracic Aortic aneurysms
| PRJNA635645 | ENA