Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from human lupus EPCs/CACs


ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Celine Berthier 

PROVIDER: E-GEOD-26950 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Inflammasome activation of IL-18 results in endothelial progenitor cell dysfunction in systemic lupus erythematosus.

Kahlenberg J Michelle JM   Thacker Seth G SG   Berthier Celine C CC   Cohen Clemens D CD   Kretzler Matthias M   Kaplan Mariana J MJ  

Journal of immunology (Baltimore, Md. : 1950) 20111104 11


Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous manifestations including severe organ damage and vascular dysfunction leading to premature atherosclerosis. IFN-α has been proposed to have an important role in the development of lupus and lupus-related cardiovascular disease, partly by repression of IL-1 pathways leading to impairments in vascular repair induced by endothelial progenitor cells (EPCs) and circulating angiogenic cells (CACs). Counterintuitively, SLE p  ...[more]

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