Please note that we have stopped the regular imports of Gene Expression Omnibus (GEO) data into ArrayExpress. This may not be the latest version of this experiment.
E-GEOD-23203 - Expression data from human healthy and lupus EPCs/CACs, and healthy CD133+ bone marrow EPCs
Released on 13 April 2011, last updated on 2 May 2014
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.
transcription profiling by array
Celine C Berthier <email@example.com>, Deborah Mattinzoli, Maria P Rastaldi, Mariana J Kaplan, Matthias Kretzler, Seth G Thacker
Inflammasome activation of IL-18 results in endothelial progenitor cell dysfunction in systemic lupus erythematosus. Kahlenberg JM, Thacker SG, Berthier CC, Cohen CD, Kretzler M, Kaplan MJ. , PMID:22058412