<HashMap><database>ENA</database><scores/><additional><omics_type>Genomics</omics_type><omics_type>Multiomics</omics_type><center_name>University of Michigan</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA136955</full_dataset_link><scientific_name>Homo sapiens</scientific_name><long_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. Overall design: 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.</long_description><tag>xref:PubMed:20805419</tag><tag>xref:PubMed:22058412</tag><repository>ENA</repository><description_synonyms>data, Disease, lupus erythematosus, human being, Libman Sacks Disease, Man (Taxonomy), Systemic, lupus, SLE, Lupus Erythematosus Disseminatus, Modern, susceptibility to, ER-PM contact site, Lupus Erythematosus, endoplasmic reticulum-plasma membrane contact junction., man, human, Human, LIBMAN SACKS DIS, Homo sapiens, Libman-Sacks Disease, ER-plasma membrane contact site, Modern Man, excess LMW-DNA, Libman-Sacks, lupus nephritis, Man, EPCS, excess lymphocyte low molecular weight DNA</description_synonyms><name_synonyms>Human, Modern., human being, Man (Taxonomy), Homo sapiens, man, Man, human, Modern Man</name_synonyms></additional><is_claimable>false</is_claimable><name>Homo sapiens</name><description>Expression data from human lupus EPCs/CACs</description><dates><last_updated>2025-09-24</last_updated><first_public>2014-02-11</first_public></dates><accession>PRJNA136955</accession><cross_references><GEO>GSE26950</GEO><taxon>9606</taxon><PubMed>20805419</PubMed><PubMed>22058412</PubMed></cross_references></HashMap>