RNA-seq of untreated and IMQ treated mouse back skin in control and Ovol1 deficient mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA664029 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12659705_1.fastq.gz | Fastqsanger.gz | |||
| SRR12659705_2.fastq.gz | Fastqsanger.gz | |||
| SRR12659706_1.fastq.gz | Fastqsanger.gz | |||
| SRR12659706_2.fastq.gz | Fastqsanger.gz | |||
| SRR12659707_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:Skin constitutes the outer permeability barrier that protects the body from dehydration and a myriad of external assaults. Epidermal keratinocytes act as the first line of innate immune defense, and barrier defects underlie common inflammatory skin diseases. However, the molecular mechanisms that maintain barrier integrity when skin is under challenge to regulate the interplay between epidermal and immune cells are not fully understood. Here we report upregulated expression of transcriptional repressorencoding Ovol1 in epidermal cells of inflamed skin, and its functional importance in maintaining barrier integrity of physically or chemically challenged skin. Following stimulation with imiquimod, Ovol1-deficient mice exhibit significantly aggravated epidermal hyperplasia and psoriasis-like skin inflammation featuring persistent neutrophil accumulation. Using bulk and single-cell RNA-sequencing, we characterize molecular changes in epidermal, fibroblasts, and immune cells that reflect altered epidermal proliferation and differentiation and/or significantly enhanced inflammatory responses as consequences of Ovol1 deletion. We identify both proliferation/differentiation-regulating and neutrophil-attracting chemokine genes as candidate direct targets of Ovol1. Finally, we provide evidence for altered IL-1a signaling in the microenvironment of Ovol1- deficient inflamed skin that functionally contributes to neutrophil accumulation and epidermal hyperplasia. Collectively, our study demonstrates a protective role for an epidermally expressed, disease-linked transcription factor in coordinating robust barrier maintenance with suppression of skin inflammation.
2021-10-27 | GSE158112 | GEO
Project description:effect of bergapten gel on IMQ mice back skin
| PRJNA853384 | ENA
Project description:We then performed gene expression profiling analysis using data obtained from RNA-seq of 9 skin tissues including 3 per group in vaseline-treated group, imq model group and bergapten-gel-treated imq model group.
2023-07-01 | GSE207059 | GEO
Project description:Imiquimod (IMQ) is a topical therapeutic immune activator that causes psoriasiform inflammation in mice. To determine if IMQ-induced inflammation and gene expression changes depended on the time of day in which treatment is administered, we performed gene expression profiling of dorsal mouse back skin by microarray after different durations of topical 1% IMQ treatment (control = no treatment, 6 hr, 24 hr, and 5 days of IMQ treatment) at different times of day (ZT01, ZT07, ZT09 = day-time treatment; ZT13 and ZT19 = night-time treatment). We also performed a time course after IMQ treatment by collecting mouse back skin after 0 (no treatment), 1, 2, 4, 6, and 24 hours post-treatment. Lastly, we determined gene expression changes in response to IMQ in mice deleted for the core circadian clock gene, Bmal1, after 0 (no treatment) and 24 hours post-1% IMQ compared to Wt (both treated and collected during the daytime at ZT09). The results of this study are important as they show that IMQ-induced activation of interferon sensitive genes are diurnal in Wt mice after 6 hours and 24 hours but not after 5 consecutive treatments. Furthermore, we find that interferon sensitive genes are induced more robustly in the skin of Bmal1 KO mice after 24 hr IMQ compared to Wt mice. These results are important for further understanding how the circadian clock regulates immune activation in response to the theraputic agent IMQ. In this dataset, we include the expression data obtained from 28 microarray samples, all of which were generated from whole back skin RNA samples pooled from 5-7 mice per sample.
2020-03-30 | GSE142165 | GEO
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:TREX2 is a keratinocyte specific 3â-deoxyribonuclease that participates in the maintenance of skin homeostasis upon damage. This transcriptome analysis identified multiple genes and pathways deregulated by TREX2 loss in the IMQ-induced psoriasis-like model in mouse skin. mRNA sequencing of 5 biological replicates of skin from wild-type mice treated with Imiquimod and 6 of Trex2 knockout mice treated with Imiquimod
2016-09-07 | E-GEOD-74528 | biostudies-arrayexpress
Project description:Skin microbiota affect systemic inflammation through mechanisms that have not been completely elucidated. We previously demonstrated that keratinocyte-specific IκBζ-deficient mice spontaneously develop autoimmune inflammation resembling human Sjögren syndrome. In this study, we examined how IκBζ-deficient epidermis dictates systemic autoimmune inflammation onset. To examine if IκBζ-deficient keratinocytes are susceptible to apoptotic stimuli in a steady state, we performed microarray analysis of untreated murine back epidermis. Data indicate that IκBζ-deficient epidermis is susceptible to environment antigens through apoptosis-related gene upregulation
2022-08-11 | GSE165515 | GEO
Project description:miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara). Gene expression profiling (Affymetrix) was used to identify transcriptomic changes associated with psoriasis-like skin inflammation in wild type vs. miR-146a -/-mice. A daily topical dose of 31.25 mg of Aldara cream (5% IMQ) was applied on the right ear of miR-146a -/- and C57BL/6 mice on three consecutive days to induce psorisis-like skin inflammation. Mice were sacrificed at day 4. Ear flaps were collected for total RNA extraction and hybridization on Affymatrix GeneTitan plate format Gene ST 2.1 (mouse).
2016-02-19 | E-GEOD-78057 | biostudies-arrayexpress
Project description:Purpose: To compare epidermal LC transcriptomes of control group (wild-type IMQ-untreated C57/BL6 mice) and IMQ group (wild-type IMQ-treated C57/BL6 mice). Results: KEGG pathway analysis implied that lesional LCs were highly enriched in several inflammatory signalling pathways, including cytokine-cytokine receptor interactions, Th1, Th2 and Th17 cell differentiation, tumor necrosis factor signalling and IL-17 signalling pathways, complement and coagulation cascades, and NOD-like receptor signalling and PI3K-Akt signalling pathways. Gene set enrichment analysis plots revealed enrichment of cytokine activity, chemoattractant activity, protein lipid complex binding, and low-density lipoprotein particle binding gene sets in LCs from IMQ+ mice compared with IMQ- mice. Conclusions: These results confirmed a proinflammatory role for epidermal LCs in the pathogenesis of psoriasis.
2020-11-28 | GSE162274 | GEO
Project description:TREX2 is a keratinocyte specific 3’-deoxyribonuclease that participates in the maintenance of skin homeostasis upon damage. This transcriptome analysis identified multiple genes and pathways deregulated by TREX2 loss in the IMQ-induced psoriasis-like model in mouse skin.
2016-09-07 | GSE74528 | GEO