Effect of bergapten gel on IMQ mice back skin
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE207059 | GEO | 2023/07/01
REPOSITORIES: GEO
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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.
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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
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Project description:Analysis of the tag densities showed lower 5-hmC levels in both CpG islands and genebodies in Imiquimod (IMQ)-treated epidermal samples. We looked further into loci-specific changes of 5-hmC and found a total of 364 differentially hydroxymethylated regions. Within these regions, 321 genes showed significantly lower 5-hmC levels and 67 genes had significantly higher 5-hmC levels in the IMQ-treated epidermis compared to control.
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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
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.
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Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare epidermal transcriptomes of control group (wild-type IMQ-untreated C57/BL6 mice), model group (wild-type IMQ-treated C57/BL6 mice) and XYF group (model group mice treated by XYF). Methods: Epidermal mRNA profiles of control group, model group and XYF group mice were generated by deep sequencing. Total RNA samples were prepared from intact epidermal ear sheets of mouse ear skin from two mice. Double-strand cDNA was generated from equal amounts of total RNA by following TruSeq8 RNA Library Prep Kit v2 (#RS-122-2001/2002, Illumina). The cDNA libraries were sequenced using Illumina Hi-seq2500. STAR software was utilized for sequence alignment between the preprocessing sequence and reference genome sequence of mice downloaded from the Ensembl database(Mus_musculus.GRCm38.90,ftp://ftp.ensembl.org/pub/release-90/gtf/mus_musculus/ Mus_musculus.GRCm38.90.chr.gtf.gz). Transcript assembly of mRNA sequencing data was performed by StringTie software. The expression levels for each of the genes were normalized to FPKM (fragments per kilobase of transcript per million fragments mapped). DESeq 2 was applied to conduct the analysis of differentially expressed genes (DEG). The cutoffs of DEG method were determined as the P value < = 0.05, the FDR value < = 0.05 and the Fold Change (FC) value > = 2. Results: Heatmap analysis of differentially expressed genes (DEG) revealed distinct transcriptomes between different groups, which displayed a partial reversal of pathological gene-expressing modifications by the treatment of XYF. Detailed comparison identified shared DEGs of opposite deviations between control group versus model group and model group versus XYF group. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis uncovered the epidermis from disease-model group was highly enriched in multiple inflammatory signaling, involving cytokine-cytokine receptor interaction, PI3K-Akt signaling pathway, IL-17 signaling pathway and cGMP-PKG signaling pathway. As for XYF therapy, PI3K-Akt signaling pathway, Calcium signaling, Hippo signaling pathway and cGMP-PKG signaling pathway were modulated in the epidermis. Further Gene Set Enrichment Analysis (GSEA) exposed downregulations in focal adhesion, ECM receptor interaction, TGF-β signaling pathway and glyoxylate and dicarboxylate metabolism in XYF-treated psoriasis-like epidermis. Conclusions: XYF might regulate various inflammatory signaling, metabolic processes and microvascular formation to influence γδT cell biology.
2020-11-10 | GSE161084 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare dermal transcriptomes of control group (wild-type IMQ-untreated C57/BL6 mice), model group (wild-type IMQ-treated C57/BL6 mice) and XYF group (model group mice treated by XYF). Methods: Dermal mRNA profiles of control group, model group and XYF group mice were generated by deep sequencing. Total RNA samples were prepared from intact dermal ear sheets of mouse ear skin from two mice. Double-strand cDNA was generated from equal amounts of total RNA by following TruSeq8 RNA Library Prep Kit v2 (#RS-122-2001/2002, Illumina). The cDNA libraries were sequenced using Illumina Hi-seq2500. STAR software was utilized for sequence alignment between the preprocessing sequence and reference genome sequence of mice downloaded from the Ensembl database(Mus_musculus.GRCm38.90,ftp://ftp.ensembl.org/pub/release-90/gtf/mus_musculus/ Mus_musculus.GRCm38.90.chr.gtf.gz). Transcript assembly of mRNA sequencing data was performed by StringTie software. The expression levels for each of the genes were normalized to FPKM (fragments per kilobase of transcript per million fragments mapped). DESeq 2 was applied to conduct the analysis of differentially expressed genes (DEG). The cutoffs of DEG method were determined as the P value < = 0.05, the FDR value < = 0.05 and the Fold Change (FC) value > = 2. Results: Heatmap analysis of differentially expressed genes (DEG) revealed distinct transcriptomes between different groups, which displayed a partial reversal of pathological gene-expressing modifications by the treatment of XYF. Detailed comparison identified shared DEGs of opposite deviations between control group versus model group and model group versus XYF group. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis uncovered the dermis from disease-model group was greatly disturbed in cytokine-cytokine receptor interaction, chemokine signaling pathways, IL-17 signaling pathway, TNF signaling pathway, Wnt signaling pathway and PI3K-Akt signaling pathway. As for XYF therapy, several metabolic pathways, Calcium signaling, cAMP signaling pathway and cGMP-PKG signaling pathway were affected within the dermis. Further Gene Set Enrichment Analysis (GSEA) exposed multiple metabolic pathways, which involved ether lipid metabolism, alpha linolenic acid metabolism, arachidonic acid metabolism, linoleic acid metabolism, glycerophospholipid metabolism, glycosaminoglycan biosynthesis heparan sulfate, along with VEGF signaling and cell cycle were considerably suppressed in the dermal tissue when given XYF. Conclusions: XYF might regulate various inflammatory signaling, metabolic processes and microvascular formation to influence γδT cell biology.
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