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Modular gene analysis reveal distinct molecular signatures for cutaneous lupus patient subsets

ABSTRACT: We utilized RNA-seq to investigate the molecular heterogenity of cutaneous lupus patients compared to controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE167923 | GEO | 2021/03/02

REPOSITORIES: GEO

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Modular gene analysis reveal distinct molecular signatures for cutaneous lupus patient subsets

Project description:Modular gene analysis reveal distinct molecular signatures for cutaneous lupus patient subsets

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Genome-wide analysis of gene expression of cutaneous lupus and cutaneous psoriasis lesions

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Spatial transcriptomics of Cutaneous and Systemic Lupus Erythematosus skin

Project description:We performed spatial transcriptomics on a case series of different clinical subtypes of cutaneous lupus erythematosus including acute cutaneous lupus erythematosus (malar rash, systemic lupus erythematosus). Our goals were to (1) determine which differentially expressed genes (DEGs) could be attributed to specific cell populations in specific locations within the tissue, (2) determine if spatial transcriptomics could better distinguish between CLE clinical subtypes than bulk RNA approaches and (3) examine potential cell-cell communication pathways within the skin lesions.

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Modular gene analysis reveals distinct molecular signatures for subsets of patients with cutaneous lupus erythematosus.

Project description:BackgroundCutaneous lupus erythematosus (CLE) is a heterogeneous autoimmune disease with clinical sequelae such as itching, dyspigmentation and scarring.ObjectivesWe applied a previously described modular analysis approach to assess the molecular heterogeneity of patients with CLE.MethodsWhole-blood transcriptomes of RNA sequencing data from a racially and ethnically diverse group of patients with CLE (n = 62) were used to calculate gene co-expression module scores. An unsupervised cluster analysis and k-means clustering based on these module scores were then performed. We used Fisher's exact tests and Kruskal-Wallis tests to compare characteristics between patient clusters.ResultsSix unique clusters of patients with CLE were identified from the cluster analysis. We observed that seven inflammation modules were elevated in two clusters of patients with CLE. Additionally, these clusters were characterized by interferon, neutrophil and cell-death signatures, suggesting that interferon-related proteins, neutrophils and cell-death processes could be driving the inflammatory response in these subgroups. Three different clusters had a predominant T-cell signature, which were supported by lymphocyte counts.ConclusionsOur data support a diverse molecular profile in CLE that further adds to the clinical variations of this skin disease, and may affect disease course and treatment selection. Future studies with a larger and diverse cohort of patients with CLE are warranted to confirm these findings.

| S-EPMC8255330 | biostudies-literature

Gene expression in cutaneous lupus erythematosus

Project description:Lesional skin biopsies were taken from patients with active, untreated lupus skin disease (chronic discoid lupus erythematosus, CDLE, n=6; subacute cutaneous lupus erythematosus, SCLE, n=5). Healthy control specimens (HC) were obtained from healthy skin of 5 patients undergoing plastic surgery. In every case, two 4mm punch biopsies were taken. One was flash-frozen in liquid nitrogen and afterwards processed for mRNA isolation. The second biopsy was fixed in 5% formalin solution overnight, and was proceeded for histological investigation.The one-color Agilent 60-mer oligo microarray (Agilent, Santa Clara, CA) was used for gene expression analyses. Statistical analyses were performed using the Agilent Feature Extraction Softwareâ¢ and the Rosetta Resolverâ¢ gene expression data analysis system. The presented gene list (Table S1) includes normalized sample/ control log10-ratios (expression > 2-fold enhanced, p<0.01).

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Targeted proteomics analysis of Cutaneous Lupus Erythematosus patient interstitial skin fluid and plasma (Neuro Exploratory panel data)

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Hypersensitive interferon responses in lupus keratinocytes reveal key mechanistic determinants in cutaneous lupus

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