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The effect of type 1 IFN on human aortic endothelial cell function in vitro: relevance to systemic lupus
John A Reynolds1, David W Ray, Leo A H Zeef
11 Arthritis Research UK Epidemiology Unit, Institute of Inflammation and Repair, Manchester Academic Health Sciences Centre, The University of Manchester , Manchester, United Kingdom .
Insights
Interferon-alpha (IFNα) does not directly impact human aortic endothelial cell function, despite its association with cardiovascular disease in systemic lupus erythematosus patients. This study found no changes in cell proliferation, network formation, or nitric oxide generation.
Area of Science:
- Cardiovascular Science
- Immunology
- Cell Biology
Background:
- Cardiovascular disease (CVD) is a significant cause of mortality in systemic lupus erythematosus (SLE) patients.
- Premature CVD in SLE is not fully understood, with interferon-alpha (IFNα) emerging as a potential contributing factor.
- IFNα is linked to both disease activity and endothelial dysfunction in SLE patients.
Purpose of the Study:
- To investigate the direct effects of IFNα on human aortic endothelial cell (HAoEC) function in vitro.
- To determine if IFNα influences HAoEC proliferation, capillary-like network formation, and nitric oxide (NO) generation.
Main Methods:
- Human aortic endothelial cells (HAoECs) were treated with IFNα2b.
- Cell proliferation, capillary-like network formation, and nitric oxide (NO) generation were assessed.
- Gene expression changes were analyzed using an exon gene array.
Main Results:
- IFNα2b regulated 198 genes, including interferon-stimulated genes (ISGs).
- Gene ontology analysis revealed enrichment in antigen presentation and host response to virus pathways.
- No significant changes were observed in HAoEC proliferation, tubule formation, or NO bioavailability.
Conclusions:
- Interferon-alpha (IFNα) in isolation does not appear to directly impact human aortic endothelial cell function.
- The findings suggest that other factors may mediate the link between IFNα and endothelial dysfunction in SLE.
Abstract:
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 the function of IFNα2b-treated HAoECs in terms of cell proliferation, capillary-like network formation, and nitric oxide (NO) generation. Changes in gene expression were also analyzed using an exon gene array. IFNα2b regulated the expression of 198 genes, including recognized interferon-stimulated genes (ISGs). Gene ontology analysis showed over-representation of genes involved in antigen presentation and host response to virus but no significant changes in clusters of genes recognized as important in endothelial cell activation or dysfunction. HAoEC proliferation, tubule formation, and NO bioavailability were unchanged, suggesting that IFNα in isolation does not have a direct impact on aortic endothelial cell function.
