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IL-17 mediated downregulation of miR-101 facilitates expression of EZH2 to promote epidermal hyperplasia in psoriasis

ABSTRACT: IL-17 mediated downregulation of miR-101 facilitates expression of EZH2 to promote epidermal hyperplasia in psoriasis

PROVIDER: PRJNA910474 | ENA |

REPOSITORIES: ENA

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IL-17 mediated downregulation of miR-101 facilitates expression of EZH2 to promote epidermal hyperplasia in psoriasis

Project description:Epidermal hyperplasia, a characteristic feature of psoriatic skin lesions, is epigenetically driven by Enhancer of Zeste homolog 2 (EZH2). EZH2 and EZH2-mediated trimethylation of histone H3 lysine 27 (H3K27me3) are both abnormally upregulated in psoriatic lesions. To identify microRNAs that could potentially target these epigenetic regulators we profiled miRNAs from psoriatic lesional skin in comparison with healthy skin. Analysis of the differentially expressed miRNAs revealed miR-101, as one of the most significant miRNA, consistently downregulated in psoriatic lesions compared to the healthy skin. A clear inverse correlation in the expression of miR-101 versus EZH2 was apparent in normal skin versus psoriatic lesional skin indicating that EZH2 is a potential target of miR-101, which was further confirmed by luciferase assay. Investigating the upstream effectors of the miR-101- EZH2 pathway in psoriasis, we identified the pro-inflammatory cytokine IL-17 as regulator of miR-101 expression. Here we propose a model, depicting a pathway triggered by IL-17 – mediated modulation of miR-101 expression, which in turn elicit sustained expression of EZH2, leading to enhanced keratinocyte proliferation and epidermal hyperplasia in psoriasis. Taken together, this indicates that miR-101 is a potential therapeutic target to alleviate the downstream effects of IL-17 mediated epidermal hyperplasia in psoriasis.

2023-09-19 | GSE220586 | GEO

Ovol1 regulates psoriasis-like skin inflammation and epidermal hyperplasia

Project description:Psoriasis is a common inflammatory skin disease characterized by aberrant inflammation and epidermal hyperplasia. Molecular mechanisms that regulate psoriasis-like skin inflammation remain to be fully understood. Here we show that the expression of Ovol1 transcription factor is upregulated in psoriatic skin, and its deletion results in aggravated psoriasis-like skin symptoms following stimulation with imiquimod (IMQ). Using bulk and single-cell RNA-sequencing, we identify molecular changes in the epidermal, fibroblast and immune cells of Ovol1-deficient skin that reflect altered course of epidermal differentiation and enhanced inflammatory responses. Furthermore, we provide evidence for excessive full-length IL-1 signaling in the microenvironment of IMQ-treated Ovol1-deficient skin that functionally contributes to immune cell infiltration and epidermal hyperplasia. Collectively, our study uncovers a protective role for Ovol1 in curtailing psoriasis-like inflammation and the associated skin pathology

2021-12-01 | GSE159704 | GEO

Ovol1 regulates psoriasis-like skin inflammation and epidermal hyperplasia

Project description:Ovol1 regulates psoriasis-like skin inflammation and epidermal hyperplasia

| PRJNA670225 | ENA

Transgenic overexpression of Pla2g2f at a level relevant to skin pathology display alopecia and psoriasis-like epidermal hyperplasia

2015-08-08 | GSE71829 | GEO

Gene expression in psoriasis lesions and uninvolved skin

Project description:Psoriasis is a chronic inflammatory skin disease characterized by marked proliferation of keratinocytes leading to pronounced epidermal hyperplasia, elongation of rete ridges and hyperkeratosis. The most common form of psoriasis, chronic plaque psoriasis (Psoriasis vulgaris), involves relatively stable occurrence and progression of sharply demarcated lesions, usually on the trunk and extremities, which share a combination of trademark histological features, including tortuous and dilated dermal capillaries, loss of the epidermal granular layer, and accumulation of neutrophils beneath parakeratotic scale. In this study, whole-genome transcriptional profiling was used to characterize gene expression in 4 lesional and uninvolved skin samples obtained from patients with stable chronic plaque psoriasis. Skin mRNA expression was analysed by microarray. Four individuals with chronic plaque psoriasis were enrolled. 6 mm punch biopsies were obtained under local anaesthesia (lidocaine) from uninvolved skin and a target plaque.

2013-12-10 | E-GEOD-50790 | biostudies-arrayexpress

Transgenic overexpression of Pla2g2f at a level relevant to skin pathology display alopecia and psoriasis-like epidermal hyperplasia

Project description:Pla2g2f is dominantly expressed in the suprabasal layer of mouse epidermis. Microarray gene profiling supported the overall tendency of epidermal and sebaceous gland hyperplasia as well as alopecia in Pla2g2f-transgenic skin. Pla2g2f-Tg/+ mice and littermate controls (C57BL/6 background); 25-day old; skin; pooled from 4 mice for each genotype.

2015-08-08 | E-GEOD-71829 | biostudies-arrayexpress

Mettl3 deficiency in epidermal keratinocytes exacerbates psoriasis-like inflammation [MeRIPseq_mice]

Project description:We analyzed epidermal samples from keratinocyte-specific knockout Mettl3 (K14CreERT2;Mettl3fl/fl) mice and their controls (Mettl3fl/fl) in imiquimod-induced psoriasis-like skin lesions. Briefly, we established an imiquimod-induced psoriasis model in K14CreERT2;Mettl3fl/fl mice and their controls after tamoxifen injection, and epidermal samples were separated and collected from the skin lesions of the mice after 3 or 6 days of modeling (n=3 per group). The aim of this study was to investigate the mechanism by which Mettl3-mediated epidermal m6A methylation affects skin inflammation.

2024-08-20 | GSE268745 | GEO

Hair follicle stem cells (HF-SCs) can initiate psoriasis-like disease in mice

Project description:Using lineage-tracing in a well-established psoriasis-like mouse model with inducible epidermal deletion of c-Jun and JunB, we found that mutant HF-SCs survive and express a broad group of pro-inflammatory cytokines, whereas mutant inter-follicular epidermal cells (IFE) disappear over time. Mutant HF-SCs initiate epidermal hyperplasia and skin inflammation by priming neighboring non-mutant epidermal cells to acquire a psoriasis-like phenotype. To explore the molecular mechanisms that govern the behavior of these distinct mutant and non-mutant HF-SCs and IFE cell populations during psoriasis-like disease, RNA sequencing analyses of sorted GFP+, Tomato+ HF-SCs and b-KCs from DKO*-mT/mG mice.

2019-08-23 | GSE119762 | GEO

Gene expression in psoriasis lesions and uninvolved skin

2013-12-10 | GSE50790 | GEO

Epigenetic silencing of SFRP4 contributes to epidermal hyperplasia in psoriasis

Project description:To investigate the gene expression of imiquimod induced psoriasis-like mouse model, we have employed whole genome microarray as a discovery platform to identify genes differentially expressed compared with wild type C57BL6 mouse exposed to the vehicle of imiquimod.

2014-08-28 | GSE60804 | GEO

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