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GSE81071
Homo sapiens
56 Downloadable Samples
Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
Cutaneous lupus erythematosus (CLE) is a disfiguring disease that can exist as an independent entity or as a manifestation of systemic lupus erythematosus (SLE) where up to 70% of patients experience lesions during their disease course. Subacute CLE (sCLE) is an inflammatory lesion with associated erythema in papulosquamous or annular formations. Typically, sCLE does not scar but depigmentation can occur. Importantly, sCLE is associated with a higher progression to SLE. Discoid lesions (DLE) are often circular and frequently lead to alopecia and scar formation. sCLE lesions have a higher propensity for photoprovocation and a more robust inflammatory infiltrate following ultraviolet (UV) B exposure. The pathogenic mechanisms which govern the differences between DLE and sCLE remain poorly defined, and this is reflected by the refractory nature of cutaneous lesions to usual lupus therapies. In this study, we evaluated the transcriptional profiles of 26 DLE and 23 sCLE biopsies and compared them to control skin and to each other in order to develop a comprehensive understanding of the similarities and differences between these two clinical subtypes.
Publication Title
Enhanced Inflammasome Activity in Systemic Lupus Erythematosus Is Mediated via Type I Interferon-Induced Up-Regulation of Interferon Regulatory Factor 1.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 33 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
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- plays a crucial role in premature vascular damage in SLE. IFN- 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- promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1 and , 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-1 promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-.
Publication Title
The detrimental effects of IFN-α on vasculogenesis in lupus are mediated by repression of IL-1 pathways: potential role in atherogenesis and renal vascular rarefaction.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Homo sapiens
- 17 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Previous studies indicate that peroxisome proliferator-activated receptor-gamma (PPAR-g) agonists suppress autoimmune responses and renal inflammation in murine lupus. However, the mechanisms implicated in this process remain unclear. We tested the effect of the PPAR-g agonist pioglitazone in human lupus and control PBMCs with regards to gene regulation and various functional assays.
Publication Title
The peroxisome-proliferator activated receptor-γ agonist pioglitazone modulates aberrant T cell responses in systemic lupus erythematosus.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
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- plays a crucial role in premature vascular damage in SLE. IFN- 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- promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1 and , 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-1 promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-.
Publication Title
The detrimental effects of IFN-α on vasculogenesis in lupus are mediated by repression of IL-1 pathways: potential role in atherogenesis and renal vascular rarefaction.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
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- plays a crucial role in premature vascular damage in SLE. IFN- 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- promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1 and , 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-1 promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-.
Publication Title
The detrimental effects of IFN-α on vasculogenesis in lupus are mediated by repression of IL-1 pathways: potential role in atherogenesis and renal vascular rarefaction.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
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- plays a crucial role in premature vascular damage in SLE. IFN- 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- promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1 and , 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-1 promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-.
Publication Title
The detrimental effects of IFN-α on vasculogenesis in lupus are mediated by repression of IL-1 pathways: potential role in atherogenesis and renal vascular rarefaction.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
Systemic sclerosis (SSc) is a rare but devastating disease of fibrosis impacting the dermis and multiple organ systems. The prevalence ranges from 4 to 489 cases per million individuals with ten year mortality rates reported around 18 percent. Survival is related to the extent of skin involvement, yet the precise mechanisms driving skin fibrosis in SSc remain unknown. In this study, we analyzed the shared and unique transcriptomic profiles of SSc and normal keratinocytes.
Publication Title
Scleroderma keratinocytes promote fibroblast activation independent of transforming growth factor beta.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 39 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
IgA nephropathy (IgAN) is the most common glomerulonephritis in the world. The disease is characterized by galactose deficient IgA (gd-IgA) in the circulation forming immune complexes. The complexes are deposited in the glomerular mesangium leading to inflammation and loss of renal function, but the pathophysiology of the disease is still not fully understood. Using an integrated global transcriptomic and proteomic profiling approach we investigated the role of the mesangium in the onset and progression of IgAN. Global gene expression was investigated by microarray analysis of the glomerular compartment of renal biopsies from patients with IgAN. The influence of galactose deficient IgA (gd-IgA) on mesangial cells was investigated by proteomic profiling. By utilizing the previous published literature curated glomerular cell type-specific genes, we found that mesangial cells and their positive standard genes play a more dominant role in IgAN comparing to the podocyte standard genes. Additionally, the patient clinical parameters (serum creatinine values and estimated glomerular filtration rate - eGFR) significantly correlate with z-scores derived from expression profile of mesangial cell positive standard genes. 22 common pathways were identified both from in vivo microarray data and in vitro mesangial cell mass spectrometry data and the main part was inflammatory pathways. The correlation between clinical data and mesangial standard genes allows for a better understanding of the onset of IgAN. The genes, proteins and their corresponding pathways identified in this paper give us novel insights into the pathophysiological mechanisms leading to progression of IgAN.
Publication Title
Transcriptomic and Proteomic Profiling Provides Insight into Mesangial Cell Function in IgA Nephropathy.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 75 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a), (ffymetrixgenechipmousegenome4302.0array[cdf:mmentrezg10)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 110 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis.
Sample Metadata Fields
Specimen part
View Samples