Ontology highlight
ABSTRACT:
PROVIDER: PRJNA645887 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12210263_1.fastq.gz | Fastqsanger.gz | |||
| SRR12210263_2.fastq.gz | Fastqsanger.gz | |||
| SRR12210264_1.fastq.gz | Fastqsanger.gz | |||
| SRR12210264_2.fastq.gz | Fastqsanger.gz | |||
| SRR12210265_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Hypoxia is used as a model for pulmonary arterial hypertension. MiR-145 is upregulated in pulmonary arterial hypertension in humans and female mice. It has been observed that miR-145 knock out mice have reduced vascular remodelling in response to hypoxia. Therefore, knock down of miR-145 could be used as a therapy for pulmonary arterial hypertension in humans. This microarray has helped us to elucidate some of the pathways in the miR-145 knock out mice that may protect against vascular remodelling. Wild type (WT) mice and homozygous miR-145 -/- female mice (strain C57BL6J/129SVEV) at 8 weeks old were exposed to chronic hypoxia for 2 weeks or maintained in normoxic conditions and pulmonary arteries were dissected at 10 weeks of age. This study contained 4 groups, WT hypoxic, WT normoxic, miR-145 -/-, hypoxic miR-145 -/- normoxic each containing 6 animals. All adjacent comparisons were made to ananlyse the data (a 2 by 2 design).
2012-05-15 | E-MTAB-885 | biostudies-arrayexpress
Project description:MicroRNA-483 (miR-483) regulate endothelial function through inhibition expression of connective tissue growth factor (CTGF). Endothelial dysfunction is involved in the pathogeneis of pulmonary arterial hypertension (PAH). We investigated the role of miR-483 overexpression on human pulmonary arterial endothelial cells (hPAECs) through comparing the transcriptome file of hPAECs transfected with miR-483 -3p and -5p mimic and with control mimic. Gene ontology analysis showed that several PAH-associated signaling pathways were regulated by miR-483, including transforming growth factor-β signaling, Wnt signaling and inflammatory response, cell adhesion, response to hypoxia, apoptotic processes, oxidative reduction processes and negative regulation of cell migration and proliferation.
2020-03-16 | GSE146774 | GEO
Project description:Microarray analysis of peripheral blood mononuclear (PBMC) cells in pulmonary arterial hypertension. Keywords = mononuclear cells Keywords = gene microarray Keywords = pulmonary arterial hypertension Keywords = Herpesvirus Keywords = biomarker Keywords: other
2003-11-15 | GSE703 | GEO
Project description:Despite recent improvements in management of idiopathic pulmonary arterial hypertension, mortality remains high. Understanding the alterations in the transcriptome–phenotype of the key lung cells involved could provide insight into the drivers of pathogenesis. In this study, we examined differential gene expression of cell types implicated in idiopathic pulmonary arterial hypertension from lung explants of patients with idiopathic pulmonary arterial hypertension compared to control lungs. After tissue digestion, we analyzed all cells from three idiopathic pulmonary arterial hypertension and six control lungs using droplet-based single cell RNA-sequencing. After dimensional reduction by t-stochastic neighbor embedding, we compared the transcriptomes of endothelial cells, pericyte/smooth muscle cells, fibroblasts, and macrophage clusters, examining differential gene expression and pathways implicated by analysis of Gene Ontology Enrichment. We found that endothelial cells and pericyte/smooth muscle cells had the most differentially expressed gene profile compared to other cell types. Top differentially upregulated genes in endothelial cells included novel genes: ROBO4, APCDD1, NDST1, MMRN2, NOTCH4, and DOCK6, as well as previously reported genes: ENG, ORAI2, TFDP1, KDR, AMOTL2, PDGFB, FGFR1, EDN1, and NOTCH1. Several transcription factors were also found to be upregulated in idiopathic pulmonary arterial hypertension endothelial cells including SOX18, STRA13, LYL1, and ELK, which have known roles in regulating endothelial cell phenotype. In particular, SOX18 was implicated through bioinformatics analyses in regulating the idiopathic pulmonary arterial hypertension endothelial cell transcriptome. Furthermore, idiopathic pulmonary arterial hypertension endothelial cells upregulated expression of FAM60A and HDAC7, potentially affecting epigenetic changes in idiopathic pulmonary arterial hypertension endothelial cells. Pericyte/smooth muscle cells expressed genes implicated in regulation of cellular apoptosis and extracellular matrix organization, and several ligands for genes showing increased expression in endothelial cells. In conclusion, our study represents the first detailed look at the transcriptomic landscape across idiopathic pulmonary arterial hypertension lung cells and provides robust insight into alterations that occur in vivo in idiopathic pulmonary arterial hypertension lungs.
2021-03-24 | GSE169471 | GEO
Project description:Pediatric pulmonary hypertension is a heterogeneous disease associated with significant morbidity and mortality. MicroRNAs have been implicated as both pathologic drivers of disease and potential therapeutic targets in pediatric pulmonary hypertension. We sought to characterize the circulating microRNA profiles of a diverse array of pediatric pulmonary hypertension patients using high throughput sequencing technology. Peripheral blood samples were drawn from patients recruited at the time of a clinically indicated cardiac catheterization and microRNA sequencing followed by differential expression and target/pathway enrichment analyses were performed. Among 63 pediatric pulmonary hypertension patients, we identified specific microRNA signatures that uniquely classified patients by disease subtype, correlated with indicators of disease severity including invasive hemodynamic metrics, and changed over the course of treatment for pulmonary hypertension. These microRNA profiles include a number of specific microRNA molecules known to function in signaling pathways critical to pulmonary vascular biology and disease, including TGFβ beta, VEGF, PI3K/Akt, cGMP-PKG, and HIF-1 signaling. Circulating levels of miR-122-5p, miR-124-3p, miR-204-5p, and miR-9-5p decreased over the course of treatment in a subset of patients who had multiple samples drawn during the study period. Our findings support the further investigation of specific microRNAs as mechanistic mediators, biomarkers, and therapeutic targets in pulmonary hypertension.
2024-10-30 | GSE280413 | GEO
Project description:miRNAs have been proved to participate in the regulation of proliferation and apoptosis in many diseases,we consider there may be associations between miRNAs and development of pulmonary arterial hypertension (PAH). Previous studies have revealed that several miRNAs participated in the regulation of the development of PAH. In this study, we investigated the miRNA differential expression spectrum in pulmonary arterial hypertension patients.
2021-10-01 | E-MTAB-10932 | biostudies-arrayexpress
Project description:Quantitative Acetylome profiling in pulmonary arterial hypertension model rats
2022-11-22 | PXD038294 |
Project description:Gene expression in the right ventricle is different in control patients as compared to either idiopathic dilated cardiomyopathy or pulmonary arterial hypertension Two human hearts obtained at autopsy from each of control, pulmonary hypertension, and dilated cardiomyopathy
2015-04-02 | E-GEOD-67492 | biostudies-arrayexpress
Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a proliferative endothelial cell phenotype, inflammation and pulmonary vascular remodeling. BMPR2 loss-of-function has been linked to pathologic plexiform lesions with obliteration of distal pulmonary arteries distal pulmonary arteries BMPR2 silencing inprimary human pulmonary artery ECs (HPAECs) recapitulate important aspects of cellular dysfunction and deregulated signaling associated with PAH. Primary HPAECs were transfected with gene-specific siRNA pools targeting BMPR2 or control siRNA followed PMA or control stimulation.
2015-12-04 | E-GEOD-70456 | biostudies-arrayexpress