Epigenetic silencing of SFRP4 contributes to epidermal hyperplasia in psoriasis
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE60804 | GEO | 2014/08/28
SECONDARY ACCESSION(S): PRJNA259596
REPOSITORIES: GEO
Similar Datasets
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. C57BL/6J mice at 6 to 8 weeks of age were applied to a daily topical dose of 62.5 mg of IMQ cream (5%) on the shaved back for 7 consecutive days. Control mice were treated with a same dose of vehicle cream.The total RNA was extracted by using TRIzol.
2014-08-28 | E-GEOD-60804 | biostudies-arrayexpress
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
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
Project description:Obesity is a risk factor for psoriasis and negatively influences the severity, treatment responsiveness, and systemic comorbidities of psoriasis. This study aimed to investigate comprehensive inflammatory changes in obesity-associated psoriasis using an obese mouse model of psoriasis induced by topical application of imiquimod or dermal injection of interleukin (IL)-23. Obese mice exhibited aggravated psoriatic dermatitis with pronounced systemic inflammatory responses when exposed to imiquimod. Notably, imiquimod-induced psoriatic dermatitis in obese mice significantly reduced fat mass. Further, pronounced monocyte–macrophage infiltration of perigonadal adipose tissue, increased expression of genes linked to inflammation, and upregulation of cell death-associated molecules were evident in obese mice treated with imiquimod compared with their lean counterparts. In contrast, IL-23 injection could induce similar features of psoriatic inflammation in obese and lean mice, without causing adipose tissue destruction or a systemic increase in inflammatory mediators. Obese adipose tissue of mice with imiquimod-induced psoriatic inflammation features genetic and epigenetic changes in adipocytes and shifts in macrophage compartments toward disturbed homeostasis using multiomic single-nucleus sequencing targeting RNA and accessible chromatin. Therefore, systemic manifestations of psoriasis, coupled with obesity-induced changes in adipose tissue, synergistically exacerbate psoriasis by disrupting the homeostatic microenvironments of adipose tissue.
2025-08-27 | GSE267866 | GEO
Project description:Here we performed single-nuclei RNAseq of the imiquimod-induced psoriasis-like mouse skin samples. This data will be useful supplementary data to the single-cell RNAseq data (GSE238086) of the imiquimod-treated mouse skin samples. Because large cells, such adipocytes, are often lost through enzymatic digestion in scRNA-seq. SnRNAseq can maximally capture and characterize the immune responses of these large cells.
2025-07-15 | GSE238085 | GEO
Project description:Psoriasis is a common chronic inflammatory skin disease. Keratinocytes (KCs) are important effector cells that can recruit inflammatory cells by releasing inflammatory factors and chemokines to promote the inflammatory cascade in psoriasis. However, the mechanism underlying KC activation in psoriasis remains unclear. Livin is an inhibitor of apoptotic proteins and its expression can directly affect the proliferation and metastasis of tumor cells. Livin expression has been reported to be significantly increased in the lesions of patients with psoriasis; however, its specific role in KC activation has not yet been reported. The aim of this study was to investigate whether livin regulates KC activation and causes the release of inflammatory mediators. The expression levels of livin in patients with psoriasis, an imiquimod (IMQ) mouse model, and M5-treated HaCaT cells were determined via immunofluorescence staining, reverse transcription-quantitative polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and western blotting. We constructed livin knockdown (Knockdown-HaCaT) and negative control (NC-HaCaT) cells using human immunodeficiency virus-1-based lentiviral vectors to study the function of livin in KCs via RNA-sequencing and proteomics analysis. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. Moreover, the effect of livin expression on the release of inflammatory mediators in KCs was verified using ELISA.
2024-05-22 | PXD035174 | Pride
Project description:Psoriasis is a common inflammatory skin disease in clinic. In order to clarify the mechanism of Longkui Yinxiao soup in treating psoriasis, we used imiquimod-induced psoriasis-like mouse model for sequencing analysis. The results showed that its mechanism of action was mainly related to lipid metabolism.
2023-03-03 | GSE226452 | GEO
Project description:Obesity has been known to be associated with psoriasis, negatively affecting its prevalence, severity, and treatment response. However, a detailed systemic inflammatory microenvironment in obesity-associated psoriasis has not been extensively investigated. To explore this further, we used a mouse model of psoriasis induced by topical application of imiquimod or injection of IL-23. We found that obese mice exhibited systemic inflammatory responses when exposed to imiquimod, with increased expression of inflammatory cytokines in the skin and elevated serum levels of mediators implicated in psoriasis pathogenesis. Notably, imiquimod also caused a significant decrease in body weight and fat, which was more pronounced in obese mice, resulting a thinner subcutaneous fat layer. Further analysis revealed higher macrophage infiltration, upregulated genes relating to the inflammatory response, and increased expression of necrosis-associated molecules in the perigonadal fat of imiquimod-treated obese mice than in lean mice. IL-23 injection induced comparable pathogenic features of psoriatic inflammation in obese and lean mice without causing adipose tissue destruction or systemic increase of inflammatory mediators.
2025-07-31 | GSE246074 | GEO
Project description:Expression data from Imiquimod-induced psoriasis mouse model
| PRJNA413303 | ENA
Project description:The polyphenol resveratrol has anti-inflammatory effects in various cells, tissues, animals and human settings of low-grade inflammation. Psoriasis is a disease of both localized and systemic low-grade inflammation. The Sirtuin1 enzyme thought to mediate the effects of resveratrol is present in skin and resveratrol is known to downregulate NF-κB; a major contributor in the development of psoriasis. Consequently we investigated whether resveratrol has an effect on an Imiquimod induced psoriasis-like skin inflammation in mice and sought to identify candidate genes, pathways and interleukins mediating the observed effects. The study consisted of three treatment groups: A control group, an Imiquimod group and an Imiquimod+resveratrol group. Psoriasis severity was assessed using elements of the Psoriasis Area Severity Index, actual skin thickness measurements, and histological examination. We performed an RNA microarray from lesional skin and afterwards Ingenuity pathway analysis to identify affected signalling pathways. Our microarray was compared to a previously deposited microarray to determine if gene changes were psoriasis-like, and to a human microarray to determine if findings could be relevant in a human setting. Imiquimod treatment induced a psoriasis-like skin inflammation. Resveratrol significantly diminished the severity of the psoriasis-like skin inflammation. The RNA microarray revealed a psoriasis-like gene expression-profile in the Imiquimod treated group, and highlighted several resveratrol dependent changes in relevant genes, such as increased expression of genes associated with retinoic acid stimulation and reduced expression of genes involved in IL-17 dependent pathways (e.g.IL-17A, IL-17F,IL-23p19 ). Quantitative PCR confirmed a resveratrol dependent decrease in mRNA levels of IL-17A and IL-19; both central in developing psoriasis. In conclusion, resveratrol ameliorates psoriasis, and changes in expression of retinoic acid stimulated genes, IL-17 signalling pathways, IL-17A and IL-19 mRNA levels in a beneficial manner suggests it might have a role in the treatment of psoriasis and should be explored further in a human setting.
2015-11-17 | GSE63684 | GEO