Ontology highlight
ABSTRACT:
PROVIDER: PRJNA984944 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25019200_1.fastq.gz | Fastqsanger.gz | |||
| SRR25019200_2.fastq.gz | Fastqsanger.gz | |||
| SRR25019201_1.fastq.gz | Fastqsanger.gz | |||
| SRR25019201_2.fastq.gz | Fastqsanger.gz | |||
| SRR25019202_1.fastq.gz | Fastqsanger.gz |
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Project description:Skin shotgun metagenomics in patients with central centrifugal cicatricial alopecia (CCCA)
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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:Central centrifugal cicatricial alopecia (CCCA) has recently been associated with increased expression of genes implicated in fibroproliferative disorders (FPDs) in the affected scalp and higher prevalence of uterine leiomyomas (UL). We therefore sought to examine the effect of UL status on the gene expression profile of the lesional scalp in CCCA patients. Scalp biopsy was obtained from 16 patients with a confirmed diagnosis of CCCA between 2017 and 2020. Microarray analysis was used to identify differential gene expression between CCCA patients with and without a history of UL. Of the 20,000 genes analyzed, 23 of 25 genes with highest expression in CCCA patients with UL held no statistical significance. No genes previously implicated in FPDs were found among the upregulated transcripts. Of all genes analyzed, only 8 upregulated genes and zero downregulated genes had a fold change >2 in CCCA patients with UL compared to CCCA patients without UL. Our findings highlight similar gene expression patterns in the scalp of CCCA patients with and without a history of UL.
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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: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:Two patients with alopecia areata were treated with systemic ruxolitinib. Skin biopsies were taken before starting treatment and 12 weeks after starting treatment. We used microarrays to assess changes in gene expression of affected skin before and after starting treatment Two patients with alopecia areata were recruited for our study. Skin biopsies of affected scalp were taken prior to starting treatment with oral ruxolinitib. Additional skin biopsies were taken 12 weeks after starting treatment. Scalp skin biopsies were taken from patients without alopecia areata for comparison. RNA was extracted, cDNA libraries were made and profiled on affymetrix microarray chips.
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