Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice
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PROVIDER: PRJNA119089 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the following subset Series: GSE17344: Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice GSE17345: Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice Refer to individual Series
2009-07-29 | E-GEOD-17365 | biostudies-arrayexpress
Project description:Expression of enzymatically inactive caspase-8, or deletion of caspase-8 from basal epidermal keratinocytes, triggers chronic skin inflammation in mice. Unlike similar inflammation resulting from arrest of NF-kB activation in the epidermal cells, the effect induced by caspase-8 deficiency did not depend on TNF, IL1, dermal macrophage function, or expression of the Toll-like receptor adapter proteins MyD88 or TRIF. Both interferon regulatory factor (IRF)3 and TANK-binding kinase were constitutively phosphorylated in the caspase-8-deficient epidermis, and knockdown of IRF3 in the epidermis-derived cells from these mice abolished the expression of upregulated genes. Temporal and spatial analyses of the alterations in gene expression that result from caspase-8 deficiency reveal that the changes are initiated before birth, around the time that cornification develops, and occur mainly in the suprabasal layer. Finally, we found that caspase-8-deficient keratinocytes display an enhanced response to gene activation by transfected DNA. Our findings suggest that an enhanced response to endogenous activators of IRF3 in the epidermis, presumably generated in association with keratinocyte differentiation, contributes to the skin inflammatory process triggered by caspase-8 deficiency. Total RNA was extracted from the dermis or epidermis derived from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice at P3. RNA from two or three mice of each genotype was pooled prior to sample processing for microarray analysis. The appropriate pairs of RNA samples suited for a direct comparison of the two different genotypes under examination were differently labeled and subsequently co-hybridized onto one microarray (dual color design).
2009-07-29 | E-GEOD-17344 | biostudies-arrayexpress
Project description:Expression of enzymatically inactive caspase-8, or deletion of caspase-8 from basal epidermal keratinocytes, triggers chronic skin inflammation in mice. Unlike similar inflammation resulting from arrest of NF-kB activation in the epidermal cells, the effect induced by caspase-8 deficiency did not depend on TNF, IL1, dermal macrophage function, or expression of the Toll-like receptor adapter proteins MyD88 or TRIF. Both interferon regulatory factor (IRF)3 and TANK-binding kinase were constitutively phosphorylated in the caspase-8-deficient epidermis, and knockdown of IRF3 in the epidermis-derived cells from these mice abolished the expression of upregulated genes. Temporal and spatial analyses of the alterations in gene expression that result from caspase-8 deficiency reveal that the changes are initiated before birth, around the time that cornification develops, and occur mainly in the suprabasal layer. Finally, we found that caspase-8-deficient keratinocytes display an enhanced response to gene activation by transfected DNA. Our findings suggest that an enhanced response to endogenous activators of IRF3 in the epidermis, presumably generated in association with keratinocyte differentiation, contributes to the skin inflammatory process triggered by caspase-8 deficiency. Epidermal keratinocytes were isolated from the skin of Casp-8F/M-bM-^@M-^SK5-Cre or Casp-8F/+K5-Cre mice. Keratinocyte samples from two mice of each genotype were isolated and subsequently cultured. Total RNA was extracted at the first and the third passage of cultivation (8 RNA samples originated in total). The appropriate pairs of RNA samples suited for a direct comparison of the two different genotypes under examination were differently labeled and subsequently co-hybridized onto one microarray (dual color design).
2009-07-29 | E-GEOD-17345 | biostudies-arrayexpress
Project description:Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice
| PRJNA123607 | ENA
Project description:Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice
| PRJNA123609 | ENA
Project description:RNA-seq of skin samples derived from Pp6fl/fl and K5.Pp6fl/fl mice
2018-11-28 | GSE123019 | GEO
Project description:Expression of enzymatically inactive caspase-8, or deletion of caspase-8 from basal epidermal keratinocytes, triggers chronic skin inflammation in mice. Unlike similar inflammation resulting from arrest of NF-kB activation in the epidermal cells, the effect induced by caspase-8 deficiency did not depend on TNF, IL1, dermal macrophage function, or expression of the Toll-like receptor adapter proteins MyD88 or TRIF. Both interferon regulatory factor (IRF)3 and TANK-binding kinase were constitutively phosphorylated in the caspase-8-deficient epidermis, and knockdown of IRF3 in the epidermis-derived cells from these mice abolished the expression of upregulated genes. Temporal and spatial analyses of the alterations in gene expression that result from caspase-8 deficiency reveal that the changes are initiated before birth, around the time that cornification develops, and occur mainly in the suprabasal layer. Finally, we found that caspase-8-deficient keratinocytes display an enhanced response to gene activation by transfected DNA. Our findings suggest that an enhanced response to endogenous activators of IRF3 in the epidermis, presumably generated in association with keratinocyte differentiation, contributes to the skin inflammatory process triggered by caspase-8 deficiency.
2009-07-29 | GSE17344 | GEO
Project description:IKKbeta is a subunit of the IkB kinase (IKK) complex required for NF-kB activation in response to pro-inflammatory signals. NF-kB regulates the expression of many genes involved in inflammation, immunity and apoptosis, and also controls cell proliferation and differentiation in different tissues; however, its function in skin physiopathology remains controversial. We here report the alterations caused by increased IKKbeta activity in basal cells of the skin of transgenic mice. Transgenic mice which express the IKKbeta gene under the control of the keratin K5 regulatory elements were generated. We analyzed back skins from wildtype and transgenic animals. Each individual array has RNA from three different mice of the same genotype.
2010-03-22 | E-GEOD-17511 | biostudies-arrayexpress
Project description:Epidermolysis bullosa simplex (EBS) is a skin disorder caused by mutations in keratin (K) 5 or K14 genes. It is widely regarded as a mechanobullous disease, resulting from a weakened cytoskeleton, causing extensive cytolysis. It was postulated by others that certain K14 mutations induce TNF-alfa and increase apoptosis. Here, we report that in K5-/- mice , the mRNA and protein levels of TNF-alfa remain unaltered. Transcriptome analysis of K5-/- mice revealed however, that the pro-inflammatory cytokines interleukin-6 and interleukin-1beta were significantly upregulated at the mRNA level in K5-/- mouse skin. These results were confirmed by TaqMan real-time PCR and ELISA assays. We hypothesize that keratin mutations contribute to EBS in a mouse model by inducing local inflammation that mediates a stress response. Experiment Overall Design: Two groups were K5-/- skin and wildtype . Six animals were included in each group. All the total RNA samples were isolated from tissues taken immediately after birth, and were pooled for later microarray experiments. Using realtime PCR and ELISA analysis confirmed our microarray result.
2008-06-15 | E-GEOD-7663 | biostudies-arrayexpress
Project description:Total RNAs extracted from skin tissues of wild-type C57BL/6 or K5-Cre;VDR f/f mice stimulated by Oxarol and their mRNA expression profiles were analyzed by RNA-sequencing
2020-03-02 | GSE145021 | GEO