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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription Profiling of Human Aortic Endothelial Cells After Treatment with Interferon-Alpha

ABSTRACT: Systemic Lupus Erythematosus is associated with an increased risk of cardiovascular disease (CVD). Interferon-response genes have been associated with endothelial dysfunction in SLE patients. The aim of this study is to identify the effects of IFN-alpha on human endothelial cells in order to determine whether IFN-alpha can directly activate the endothelium.

ORGANISM(S): Homo sapiens

SUBMITTER: Leo Zeef

PROVIDER: E-MEXP-3746 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The effect of type 1 IFN on human aortic endothelial cell function in vitro: relevance to systemic lupus erythematosus.

Reynolds John A JA Ray David W DW Zeef Leo A H LA O'Neill Terence T Bruce Ian N IN Alexander M Yvonne MY

Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 20140120 5

Cardiovascular disease (CVD) is an important cause of morbidity and mortality in patients with systemic lupus erythematosus. The etiopathogenesis of premature CVD is not fully understood, but recently interferon-alpha (IFNα) has been implicated as a contributing factor. Since IFNα has been associated with both disease activity and endothelial dysfunction in lupus patients, we aimed to determine whether IFNα has direct effects on human aortic endothelial cell (HAoEC) function in vitro. We studied ...[more]

PMID: 24444308

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Transcription profiling of certolizumab pegol attenuation of the proinflammatory state in endothelial cells

Project description:Rheumatoid arthritis (RA) is associated with accelerated atherosclerosis and premature cardiovascular death. Anti-TNF therapy is thought to reduce clinical cardiovascular disease risk and improve vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to explore the effects of certolizumab pegol (CZP) on TNF-activated human aortic endothelial cells (HAoECs. HAoECs were cultured in vitro and exposed to i) TNF alone, ii) TNF plus CZP, or iii) neither agent followed by transcription profiling.

2012-11-16 | E-MEXP-3540 | biostudies-arrayexpress

RNA-seq of primary aortic human endothelial cells before and after TNFα stimulation

Project description:To characterize the transcriptome of primary vascular endothelial cells (ECs) during TNFα-response, we performed total RNA-seq on primary human aortic ECs (HAEC), before and after TNFα (45 min. 10 ng/mL).

2020-06-01 | E-MTAB-7896 | biostudies-arrayexpress

AP-MS of ALPK3 in cardiomyocytes

Project description:Pathogenic mutations in alpha kinase 3 (ALPK3) cause cardiomyopathy and a range of musculoskeletal defects. How ALPK3 mutations result in disease remains unclear and little is known about this atypical kinase. Using a suite of engineered human pluripotent stem cells (hPSCs) we show that ALPK3 localizes to the sarcomere, specifically at the M-Band. Both sarcomeric organization and calcium kinetics were disrupted in ALPK3 deficient hPSC derived cardiomyocytes. Further, cardiac organoids derived from ALPK3 knockout hPSCs displayed reduced force generation. Phosphoproteomic profiling of wildtype and ALPK3 null hPSC derived cardiomyocytes revealed ALPK3-dependant phospho-peptides were enriched for proteins involved in sarcomere function and protein quality control. We demonstrate that ALPK3 binds to the selective autophagy receptor SQSTM1 (Sequestome 1) and is required for the sarcomeric localization of SQSTM1. We propose that ALPK3 is a myogenic kinase with an integral role in the intracellular signaling networks underlying sarcomere maintenance required for continued cardiac contractility.

2023-01-19 | PXD035734 | Pride

Expression data from human healthy and lupus EPCs/CACs, and healthy CD133+ bone marrow EPCs

Project description:Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that interferon-α plays a crucial role in premature vascular damage in SLE. IFN-α alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). Here we demonstrate that IFN-α promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1α and β, IL-1 receptor 1 and vascular endothelial growth factor A (VEGF-A) and upregulation of IL-1 receptor antagonist (IL-1RN) and the decoy receptor IL1-R2. IL-1β promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-α. We used microarrays to analyze the effect of IFNα on peripheral blood EPCs/CACs and on bone marrow EPCs exposed to proangiogenic stimulation. This SuperSeries is composed of the SubSeries listed below. Human healthy and lupus EPCs and CACs from PBMCs, and healthy EPCs from bone marrow, were isolated and cultured under proangiogenic stimulation; after IFN-α incubation or not, RNA was extracted and processed for hybridization on Affymetrix microarrays.

2011-04-13 | E-GEOD-23203 | biostudies-arrayexpress

Expression data from human healthy CD133+ bone marrow EPCs

Project description:Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that interferon-α plays a crucial role in premature vascular damage in SLE. IFN-α alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). Here we demonstrate that IFN-α promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1α and β, IL-1 receptor 1 and vascular endothelial growth factor A (VEGF-A) and upregulation of IL-1 receptor antagonist (IL-1RN) and the decoy receptor IL1-R2. IL-1β promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-α. We used microarrays to analyze the effect of IFNα on peripheral blood EPCs/CACs and on bone marrow EPCs exposed to proangiogenic stimulation. Human healthy EPCs from bone marrow were isolated and cultured under proangiogenic stimulation; after IFNa incubation or not, RNA was extracted and processed for hybridization on Affymetrix microarrays.

2011-04-13 | E-GEOD-26951 | biostudies-arrayexpress

Transcription profiling of human endothelial and fibroblast cells isolated from umbilical cord veins treated with interferons to identify genes regulated by interferons

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2009-04-08 | E-GEOD-3920 | biostudies-arrayexpress

Expression data from human lupus EPCs/CACs

Project description:Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that interferon-α plays a crucial role in premature vascular damage in SLE. IFN-α alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). Here we demonstrate that IFN-α promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1α and β, IL-1 receptor 1 and vascular endothelial growth factor A (VEGF-A) and upregulation of IL-1 receptor antagonist (IL-1RN) and the decoy receptor IL1-R2. IL-1β promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-α. We used microarrays to analyze the effect of IFNα on peripheral blood EPCs/CACs and on bone marrow EPCs exposed to proangiogenic stimulation. Human lupus EPCs and CACs from PBMCs were isolated and cultured under proangiogenic stimulation; after IFNa incubation or not, RNA was extracted and processed for hybridization on Affymetrix microarrays.

2011-04-13 | E-GEOD-26950 | biostudies-arrayexpress

The effect of fenofibrate on endothelial cells

Project description:Fenofibrate is a synthetic ligand for the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha, but there are reports that fenofibrate affects endothelial cells in PPARa-independent manner. In order to identify PPARa-dependently and PPARa-independently regulated transcripts we generated microarray data from human endothelial cells treated with fenofibrate with and without siRNA-mediated knock-down of PPARa. In this study, we generated microarray data from human umbilical vein endothelial cells (HUVECs) treated with fenofibrate. Time 0 indicates the start point of observation immediately prior to exposure to the 25umol fenofibrate. There are five time points (2, 4, 6, 8, and 18hours) (n=3 at each time point). The control is untreatment HUVEC (n=4).

2010-05-06 | E-GEOD-15483 | biostudies-arrayexpress

ATAC-seq of primary mammalian aortic endothelial cells before and after TNFα stimulation

Project description:To identify conserved TNFα-induced changes in chromatin-accessibility in mammals, we performed ATAC-seq in primary vascular endothelial cells (ECs) isolated from the aortas of human (HAEC), mouse (MAEC) and cow (BAEC), before and after TNFα. We overlay our data with multi-species NF-κB binding data and identify multiple modes of NF-κB-chromatin interactions that are conserved during mammalian TNFα response. Our cross-species approach identifies conserved changes in chromatin-accessibility at NF-κB binding sites that are disease-relevant and essential during mammalian acute inflammation.

2020-06-01 | E-MTAB-7878 | biostudies-arrayexpress

Increased Cell Surface Fas Expression is Necessary to Sensitize Lung Fibroblasts to Fas Ligation-Induced Apoptosis: Implications for Fibroblast Accumulation in Idiopathic Pulmonary Fibrosis.

Project description:Idiopathic pulmonary fibrosis (IPF) is associated with the accumulation of collagen-secreting fibroblasts and myofibroblasts in the lung parenchyma. Many mechanisms contribute to their accumulation, including resistance to apoptosis. In previous work, we showed that exposure to the pro-inflammatory cytokines, TNF-α and IFN-γ reverses fibroblast resistance to apoptosis. The goal of this study was to investigate the underlying mechanism. Based on an initial interrogation of the transcriptomes of unstimulated and TNF-α and IFN-γ-stimulated primary lung fibroblasts and the lung fibroblast cell line, MRC5, we show here that among Fas-signaling pathway molecules, Fas expression was increased ~6-fold in an NF-κB and p38mapk-dependent fashion. Prevention of the increase in Fas expression using Fas siRNAs blocked the ability of TNF-α and IFN-γ to sensitize fibroblasts to Fas ligation induced-apoptosis; while enforced adenovirus-mediated Fas overexpression was sufficient to overcome basal resistance to Fas-induced apoptosis. Examination of lung tissues from IPF patients revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci. Collectively, these findings suggest that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis. They also suggest that approaches aimed at increasing Fas expression by lung fibroblasts and myofibroblasts may be therapeutically relevant. To investigate the mechanism by which TNF-α and IFN-γ reprogram fibroblasts from resistance to sensitivity to Fas-ligation-induce apoptosis, we exposed human primary lung fibroblasts from an IPF patient (FS087) and non-disease control subject (N78) and the human fetal lung fibroblast cell lung (MRC-5) to TNF-α (10 ng/ml) and IFN-γ (50 U/ml) for 36 hr and analyzed changes in their transcriptomes using Affymetrix microarrays.

2011-01-13 | E-GEOD-26594 | biostudies-arrayexpress

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