Expression data from Imiquimod-induced psoriasis mouse model
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ABSTRACT:
PROVIDER: PRJNA413303 | ENA |
REPOSITORIES: ENA
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Project description:Psoriasis is a chronic inflammatory skin disorder that is predominantly characterized by sharply demarcated chronic erythematous plaques. Although its etiological mechanisms are largely unknown, recent evidence suggests that the topical application of imiquimod (IMQ) cream causes psoriasis-like skin inflammation in humans and mice. Skin examined 4 hours after IMQ cream treatment. Results provide insight into the role of each knockout mice phenotype in the response to IMQ-induced psoriasis model.
2017-10-06 | GSE104603 | GEO
Project description:Molecular analysis in imiquimod (IMQ)-induced psoriasis model
| PRJNA639875 | ENA
Project description:The mechanisms underlying pruritus of imiquimod (IMQ)-induced psoriasis remain poorly understood. In this study, we investigated whether there are certain key signaling molecules downstream of the recently identified peptides mediating itch in the spinal cord. We investigated the changes in the trascriptome by performing RNAseq of cervical spinal cords in control and IMQ-induced psoriasis. Our study represents the detailed analysis of transcriptomes of spinal cord in chronic itch model with biologic replicates, generated by RNA-seq technology.
2023-06-15 | GSE152637 | GEO
Project description:We provide a new psoriasis mouse model which is induced by p38 activation in skin. We compared the individual transcriptomic profiles of anisomycin and imiquimod-induced dermatitis. We used microarrays to compare the gene expression pattern between anisomycin- and imiquimod- induced dermatitis.
2019-02-15 | GSE110658 | GEO
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
Project description:This dataset contains quantitative, bottom-up DIA proteomics data generated as part of a larger study entitled "AI-Guided CRISPR Screen Reveals Repurposed Drugs as Topical Psoriasis Therapeutics," and is organized into two complementary sub-studies.Sub-study 1 – Pharmacological Rescue in a Mouse Psoriasis ModelThe first proteomics component was designed to molecularly characterize pharmacological rescue effects in an imiquimod (IMQ)-induced mouse psoriasis model following prioritization of candidate targets from a CRISPR-based genetic screen. Mouse skin samples were collected from five experimental conditions: untreated control, IMQ only, IMQ plus the ALOX5 inhibitor zileuton, IMQ plus the OXTR antagonist cligosiban, and IMQ plus an IL-17RA blocking antibody serving as a positive control. Skin tissues were processed for bottom-up proteomics and analyzed using dia-PASEF on a timsTOF Ultra 2 mass spectrometer coupled to an Evosep One liquid chromatography system. Proteomic data were analyzed using DIA-NN in library-free mode against a SwissProt-reviewed Mus musculus reference proteome (Mouse_SwissProt_CanonicalAndIsoform_20250324.fasta). The resulting protein-level quantitative dataset enables assessment of molecular pathways associated with IMQ-driven inflammation and the extent to which these signatures are modulated or rescued by pharmacological intervention.Sub-study 2 – CRISPR Knockout Proteomics in Human KeratinocytesThe second proteomics component was designed to characterize the proteomic consequences of genetically ablating the candidate therapeutic targets ALOX5 and OXTR in a human cellular psoriasis-relevant context. Human keratinocytes were subjected to CRISPR-mediated knockout of either ALOX5 or OXTR and compared against wild-type controls. Samples were processed for bottom-up proteomics and analyzed using dia-PASEF on a timsTOF Ultra 2 mass spectrometer coupled to an Evosep One liquid chromatography system. Proteomic data were analyzed using DIA-NN in library-free mode against a SwissProt-reviewed Homo sapiens reference proteome. The resulting dataset enables assessment of the downstream molecular signatures driven by loss of each target in human keratinocytes.
2026-05-21 | PXD071833 | 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:We investigated the regulatory role of alloferon in the development of psoriasis in an imiquimod (IMQ)-induced psoriasis model through the regulation of IL-22Rα expression. Psoriasis is an immune-mediated inflammatory skin disease. IL-22, a proinflammatory cytokine, is implicated in psoriasis pathogenesis; however, there is currently no established biological treatment targeting IL-22 or its receptor, IL-22Rα. Alloferon is a short peptide that has an anti inflammatory effect on skin disorders; however, little is known about its anti-inflammatory activity in psoriasis. This study demonstrate that alloferon could be an effective potential drug for the treatment of psoriasis by interrupting IL-22 signaling and factors related to skin inflammation.
2025-03-05 | GSE285640 | 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:Single-cell RNA-seq of isolated non-parenchymal cells from imiquimod-induced psoriasis mouse model.
| PRJNA1285919 | ENA