Mus musculus strain:C57BL6N
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ABSTRACT:
PROVIDER: PRJNA700976 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mineralocorticoid receptor dependent gene expression in cardiac endothelial cells
| PRJNA972993 | ENA
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:Impact of the mineralocorticoid receptor on differential gene expression in endothelial cells
| PRJNA427260 | ENA
Project description:Effect of Mineralocorticoid Receptor deletion on glucocorticoid signalling in the macropahge
| PRJNA131199 | ENA
Project description:We explored the impact of transforming growth factor β receptor III (TGFBR3) knockdown on the gene expression in the human pulmonary arterial endothelial cells (hPASMC).
2017-12-16 | GSE92553 | GEO
Project description:To elucidate the aldosterone-regulated genes in vascular endothelial cells, we developed human endothelial cell line (EAhy926) stably expressing human mineralocorticoid receptor by retroviral system (MR-EAhy). Then gene expression profile of MR-EAhy stimulated with or without aldosterone was compared using DNA microarray analysis.
2011-03-18 | GSE28009 | GEO
Project description:CD157 marks tissue resident vasculoreparative endothelial stem cells
| PRJDB6281 | ENA
Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. The levels of senescence marker, p16INK4A and senescence-associated β-galactosidase (SA-β-gal) activity are higher in PA endothelial cells (ECs) isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16fl/fl-Cdh5(PAC)-CreERT2 (p16iΔEC) mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing platelet-derived growth factor (PDGFB) expression. Transcriptomic analyses of IPAH patient or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and their interaction with TWIST1. Knockdown of p16INK4A attenuates the expression of PDGFB and TWIST1 in IPAH patient PAECs or hypoxia-treated mouse lungs and suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel implanted on the mouse lungs. Hypoxia-treated mouse lung EC-derived exosomes stimulate DNA synthesis and migration of PASMCs in vitro and in the gel implanted on the mouse lungs, while p16iΔEC mouse lung EC-derived exosomes inhibit the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.
2022-10-15 | PXD033549 | Pride
Project description:Journal : Blood. 2009 Jul 9;114(2):469-77. Epub 2009 May 13. Title : Endothelial deletion of hypoxia-inducible factor-2alpha (HIF-2alpha) alters vascular function and tumor angiogenesis. Authors : Skuli N, Liu L, Runge A, Wang T, Yuan L, Patel S, Iruela-Arispe L, Simon MC, Keith B. Abstract : Hypoxia-inducible factor-2alpha (HIF-2alpha) is highly expressed in embryonic vascular endothelial cells (ECs) and activates the expression of target genes whose products modulate vascular function and angiogenesis. In this report, we describe a genetic model designed to test the physiologic consequences of deleting HIF-2alpha in murine endothelial cells. Surprisingly, mice with HIF-2alpha-deficient ECs developed normally but displayed a variety of phenotypes, including increased vessel permeability, aberrant endothelial cell ultrastructure, and pulmonary hypertension. Moreover, these animals exhibited defective tumor angiogenesis associated with increased hypoxic stress and tumor cell apoptosis. Immortalized HIF-2alpha-deficient ECs displayed decreased adhesion to extracellular matrix proteins and expressed reduced levels of transcripts encoding fibronectin, integrins, endothelin B receptor, angiopoietin 2, and delta-like ligand 4 (Dll4). Together, these data identify unique cell-autonomous functions for HIF-2alpha in vascular endothelial cells. Keywords: Murine lung endothelial cell study Cnt1,2 and 3 (Hif-2a floxed/floxed) cells were subjected to 0.5% oxygen treatment for 16hrs and KO1,2 and 3 (Hif-2a knockout) cells were subjected to 0.5% oxygen treatment for 16hrs.
2009-07-15 | E-GEOD-16067 | biostudies-arrayexpress
Project description:Pulmonary arterial hypertension (PAH) is a progressive fatal disease that is characterized by pathological pulmonary artery remodeling, in which endothelial cell (EC) dysfunction is critically involved. We herein describe a previously unknown role of endothelial angiocrine in pulmonary hypertension. By searching for genes highly expressed in lung microvascular ECs, we identified inhibin--A (INHBA) as an angiocrine factor produced by pulmonary capillaries. We found that excess production of INHBA by ECs impairs the endothelial function in an autocrine manner by functioning as activin A (ActA). Mechanistically, ActA induces bone morphogenetic protein receptor type 2 (BMPRII) internalization and targeting to lysosomes for degradation, resulting in BMPRII signal deficiency in ECs. When endothelial ActA-BMPRII link is overdriven in mice, hypoxia-induced pulmonary hypertension was exacerbated, whereas conditional knockout of INHBA in ECs prevents the progression of pulmonary hypertension. These data collectively indicate a critical role for the dysregulated endothelial ActA-BMPRII link in the progression of pulmonary hypertension, and thus endothelial INHBA/ActA is an attractive pharmacotherapeutic target for the treatment of PAH.
2020-12-15 | GSE156233 | GEO