Gene expression analysis of frozen skin from B6 mouse models of Cutaneous Lupus Erythematosus and Primary Cicatricial Alopecia
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PROVIDER: PRJNA1206719 | ENA |
REPOSITORIES: ENA
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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 Software⢠and the Rosetta Resolver⢠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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Project description:Gene Expression Profile of Central Centrifugal Cicatricial Alopecia
| PRJNA449869 | ENA
Project description:Background: Central Centrifugal Cicatricial Alopecia (CCCA) is a primary cicatricial alopecia that most commonly affects women of African descent. Like CCCA, fibroproliferative disorders (FPDs) such as keloids, atherosclerosis and fibroids, are characterized by low-grade inflammation and irritation resulting in end stage fibrosis. Objective: We sought to determine if fibroproliferative genes were upregulated in patients with CCCA Methods: Five patients with biopsy proven CCCA were recruited for this study. Two scalp biopsies were obtained from each patient; one from CCCA affected vertex scalp and one from the unaffected occipital scalp. Microarray analysis was performed to determine the differential gene expression patterns Results: Several pathways responsible for excess collagen deposition and aberrant wound healing were up-regulated in CCCA affected scalp when compared to unaffected scalp with patterns similar to other FPDs. Genes downregulated in CCCA affected tissue included those with roles in lipid metabolism and fatty acid biosynthesis. Limitations: Small sample size and the use of whole skin tissue for analysis. Conclusion: We have identified the up-regulation of critical genes implicated in fibroproliferative disorders in the gene expression profile of patients with CCCA. These findings may help identify future therapeutic targets for this otherwise difficult to treat condition.
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Project description:The hair follicle stem cell niche is an immune-privileged microenvironment, characterized by reduced antigen presentation, thus shielding against permanent immune-mediated tissue damage. In this study, we demonstrated the protective role of hair follicle-specific epidermal growth factor receptor (EGFR) against scarring hair follicle destruction. Mechanistically, disruption of EGFR signalling generated a cell-intrinsic hypersensitivity within the JAK-STAT1 pathway, which, synergistically with interferon gamma expressing CD8 T-cell and NK-cell-mediated inflammation, compromised the stem cell niche. Hair follicle-specific genetic depletion of either JAK1/2 or STAT1 or therapeutic inhibition of JAK1/2 ameliorated the inflammation, restored skin barrier function and activated the residual stem cells to resume hair growth in mouse models of epidermal and hair follicle-specific EGFR deletion. Skin biopsies from EGFR inhibitor-treated and cicatricial alopecia patients indicated active STAT1 signalling and interferon target expression. Notably, a case study of folliculitis decalvans, characterized by progressive hair loss, scaling and perifollicular erythema, demonstrated successful treatment with JAK1/2 inhibition. Our findings offer molecular insights and present a mechanism-based therapeutic strategy for addressing chronic folliculitis associated with EGFR-inhibitor anti-cancer therapy and cicatricial alopecia.
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Project description:Autoimmune alopecia is a prevalent, highly morbid disease. The inflammatory pathways causing hair loss are not well characterized. We profiled two tissue microarrays comparing healthy skin to scarring alopecia and alopecia areata via spatial transcriptomics to analyze the genes and pathways dysregulated in autoimmune alopecia in direct proximity to the hair follicle.
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