Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA92473 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cultures of human aortic (HAEC) and pulmonary artery endothelial cells (HPAEC) were exposured to short-term chronic hypoxia (1% O2) for either 0h, 8h or 24h Keywords: Time course, cell-type comparison The response of each cell type (HAEC and HPAEC) to short-term chronic hypoxia was determined by a single SAGE library for each of three time points (0h, 8h and 24h)
2005-06-28 | E-GEOD-2838 | biostudies-arrayexpress
Project description:Cultures of human aortic (HAEC) and pulmonary artery endothelial cells (HPAEC) were exposured to short-term chronic hypoxia (1% O2) for either 0h, 8h or 24h Keywords: Time course, cell-type comparison
2005-06-28 | GSE2838 | GEO
Project description:Physiological shear stress, produced by blood flow, homeostatically regulates the phenotype of pulmonary endothelial cells exerting anti-inflammatory and anti-thrombotic actions and maintaining normal barrier function. In the pulmonary circulation hypoxia, due to high altitude or diseases such as COPD, causes vasoconstriction, increased vascular resistance and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of this pulmonary hypertension. However, the direct interactive effects of hypoxia and shear stress on the pulmonary endothelial phenotype have not been extensively studied. We cultured human pulmonary microvascular endothelial cells (HPMEC) in normoxia or hypoxia while subjected to physiological shear stress or in static conditions. Unbiased proteomics was used to identify hypoxia-induced changes in protein expression. Using publicly available single cell RNA-seq datasets, differences in gene expression between the alveolar endothelial cells from COPD and healthy lungs were identified. 60 proteins were identified in HPMEC lysates whose expression changed in response to hypoxia in sheared but not in static conditions. mRNA for five of these (ERG, MCRIP1, EIF4A2, HSP90AA1 and DNAJA1) showed similar changes in the endothelial cells of COPD compared to healthy lungs. These data show that the proteomic responses of the pulmonary microvascular endothelium to hypoxia are significantly altered by shear stress and suggest that these differences are important in the development of hypoxic pulmonary vascular disease.
2023-02-17 | PXD036260 | Pride
Project description:SAGE analysis of human glomerular endothelial cell
| PRJNA134055 | ENA
Project description:Dysfunction of pulmonary arterial endothelial cells (PAECs) is associated with the development and progression of vascular pathology. However, it remains unknown how pulmonary hypertension (PH) affects cellular composition and transcriptomic profile of pulmonary endothelium. Here, we have undertaken a single-cell, compartment specific approach to characterise alterations in PAECs associated with two different types of PH, i.e., pulmonary arterial hypertension (PAH) and pulmonary hypertension associated with pulmonary fibrosis (PHPF). Our unbiased analysis showed that endothelium of medium / small caliber pulmonary arteries is composed of three subsets of endothelial cells (ECs). The analysis of healthy and PH endothelium revealed that the three populations are persistently represented in remodelled arteries. Additionally, an exploratory analysis of human aorta (AO) and coronary arteries (CA) endothelium revealed that, although similar gene expression patterns were noticeable, PAECs subpopulations proportions differs significantly from pulmonary arteries (PA) endothelium. To address whether EC heterogeneity is a prime feature of human endothelium, we also performed a similar analysis in a murine model of hypoxia, revealing that similar EC populations were evident in this animal model. Comparative analysis of EC subpopulations in healthy and PH EC identified a common genetic deregulation accompanying vascular remodelling. Even though murine EC displayed some similarities with human EC subpopulations, the intense re-programming associated with hypoxia associated vascular remodelling displayed significant differences compared to the human disease. Finally, in depth comparative analysis of PAH and PHPF EC highlighted the development of disease-specific transcriptomic alterations in the three populations. Therefore, characterisation of transcriptomic differences in the endothelial bed of PAH and PHPF patients can facilitate identification of novel, disease-specific therapeutic targets.
2024-07-11 | GSE228643 | GEO
Project description:Regulation of coding and non-coding genes is studied from primary human aortic endothelial cells (HAECs), venous endothelial cells (HUVECs), aortic smooth muscle cells (HASMCs) and macrophages (CD14+) under pro-atherogenic stimuli (hypoxia, oxPAPC and hypoxia+oxPAPC) by integrating three different sequencing techniques: GRO-seq, miRNA-seq and RNA-seq.
2021-05-14 | GSE154427 | GEO
Project description:Regulation of coding and non-coding genes is studied from primary human aortic endothelial cells (HAECs), venous endothelial cells (HUVECs), aortic smooth muscle cells (HASMCs) and macrophages (CD14+) under pro-atherogenic stimuli (hypoxia, oxPAPC and hypoxia+oxPAPC) by integrating three different sequencing techinques: GRO-seq, miRNA-seq and RNA-seq
2020-06-17 | GSE136813 | GEO
Project description:Gene expression profiling of HUVEC (human umbilical vein EC cell; Lonza), HAEC (human aortic EC cells), HCAEC (human coronary artery EC cells), HPAEC (human pulmonary artery EC cells), HMVEC (human microvascular (dermal) , HASMC ( Human Aortic Smooth Muscle Cells), T cells and Bcells. Gene expression profiling of Endothelial cells and Non-endothelial cells in order to identify the genes with preferntial expression to endothelial cells. The experiments are performed in duplicate on both the HT Human Genome U133A and U133B arrays.
2011-04-04 | E-GEOD-21212 | biostudies-arrayexpress
Project description:Pulmonary hypoxia is a common complication of chronic lung diseases leading to the development of pulmonary hypertension. The underlying sustained increase in vascular resistance in hypoxia is a response unique to the lung. Thus, we hypothesised that there are genes whose expression is altered selectively in the lung in response to alveolar hypoxia. Using a novel subtractive array strategy, we compared gene responses to hypoxia in primary human pulmonary microvascular endothelial cells to those in cardiac microvascular endothelium and identified genes selectively differentially regulated in the lung endothelium. Keywords: Time course, cell type comparison
2008-11-21 | GSE11341 | GEO