Expression data from adult mice pulmonary endothelial cells
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ABSTRACT:
PROVIDER: PRJNA532730 | ENA |
REPOSITORIES: ENA
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Project description:A number of mediators that have been found to be involved in the pathogenesis of hypoxic pulmonary hypertension, these mediators including mRNA, microRNAs and long noncoding RNAs. Endothelial dysfunction plays a major role in the initiation of pulmonary vascular remodeling and is thought to be a major contributor to this process. However, mRNA and no-coding RNAs expression profiles and their biological functions in pulmonary artery endothelial cells (PAECs) exposed to hypoxia need to be investigated further. Pulmonary artery endothelial cells (PAECs) were exposed to normoxia condition (21% O2, 5% CO2, 74% N2) or hypoxia condition (3% O2, 5% CO2, 92% N2) (n=3 for each group).PAECs were harvested after 24 hours and performed to further analysis.
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Project description:Pulmonary arterial hypertension (PAH) is a severe and incurable pulmonary vascular disease. One of the primary origins of PAH is pulmonary endothelial dysfunction leading to vasoconstriction, aberrant angiogenesis and smooth muscle cell proliferation, endothelial-to-mesenchymal transition, thrombosis and inflammation. Our objective was to study the epigenetic variations in pulmonary endothelial cells (PEC) through a specific pattern of DNA methylation. DNA was extracted from cultured PEC from patients with idiopathic PAH (n=11), heritable PAH (n=10) and controls (n=18). ). DNA methylation was assessed using the Illumina HumanMethylation450 Assay. After normalization, samples and probes were clustered according to their methylation profile. Differential clusters were functionally analysed using bioinformatics tools.
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Project description:Early postnatal life is considered as a critical time window for determination of long-term metabolic states and organ functions. Extrauterine growth restriction (EUGR) causes the development of adult onset chronic diseases, including pulmonary arterial hypertension (PAH). However, the effects of nutritional disadvantages during early postnatal period on pulmonary vascular consequences in later life are not fully understood. Our study was designed to test whether epigentic dysregulation mediates the cellular memory of this early postnatal event. To test this hypothesis, we isolated pulmonary vascular endothelial cells (PVEC) by magnetic-activated cell sorting (MACS) from EUGR and control rats. A postnatal insult, nutritional restriction-induced EUGR caused development of an increased pulmonary artery pressure at 9-week of age in male rats. MeDIP-chip (Methyl-DNA immune precipitation chip), genome-scale mapping studies to search for differentially methylated loci between control and EUGR rats revealed significant difference in cytosine methylation between EUGR and control rats. We validated candidate dysregulated loci with quantitative assays of cytosine methylation and gene expressions. EUGR changes cytosine methylation at ~500 loci in male rats at 9 weeks of age, preceding the development of PAH and these represent candidate loci for mediating the pathogenesis of pulmonary vascular disease that occurs later in life. These results demonstrate that epigenetic dysregulation is a strong mechanism for propagating the cellular memory of early postnatal events, causing changes in expression of genes and long term susceptibility to PAH, and further providing a new insight into prevention and treatment of EUGR-related PAH. MeDIP together with microarray analysis demonstrated that significant differences in cytosine methylation between EUGR and control rats. Comparison of EUGR(n=3) vs Control (n=3) male rats' pulmonary vascular endothelial cells in 9-week age old rats
2013-07-10 | E-GEOD-48648 | biostudies-arrayexpress
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Project description:Dilated cardiomyopathy is a frequently occurring human disease compromising heart function and a major cause of cardiac death. The causes of cardiomyopathies are often unknown. There is increasing evidence indicating that endothelial cells lining blood vessels control the homeostasis of various organs, but the special properties and functional roles of the vasculature in the adult heart maintain remain little understood. Here, we have used mouse genetics, imaging and cell biology approaches to investigate how vascular homeostasis in the adult heart is controlled by EphB4 and its ligand ephrin-B2, which are known regulators of sprouting angiogenesis, vascular morphogenesis and arteriovenous differentiation during development. We show that inducible and endothelial cell-specific inactivation of the Ephb4 gene in adult mice is compatible with survival, but leads to rupturing of cardiac capillaries, cardiomyocyte hypertrophy, and pathological cardiac remodelling. In contrast, EphB4 is not required for the integrity and homeostatic function of capillaries in skeletal muscle. Our analysis of mutant mice and cultured endothelial cells shows that EphB4 controls the function of caveolae, cell-cell adhesion under mechanical stress and lipid transport. Together, our findings establish that EphB4 maintains critical functional properties of the adult cardiac vasculature and thereby prevents dilated cardiomyopathy-like defects.
2019-11-20 | PXD012575 | Pride
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.
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