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Omics score: 3

Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

ABSTRACT: 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

OTHER RELATED OMICS DATASETS IN: PRJNA123609PRJNA119089PRJNA123607

ORGANISM(S): Mus Musculus

SUBMITTER: Oliver Dittrich-Breiholz

PROVIDER: E-GEOD-17365 | ArrayExpress | 2009-07-29

SECONDARY ACCESSION(S): GSE17365PRJNA119089

REPOSITORIES: GEO, ArrayExpress

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			Action	DRS
	E-GEOD-17365.README.txt	Txt
	E-GEOD-17365.idf.txt	Idf
	E-GEOD-17365.processed.1.zip	Processed
	E-GEOD-17365.raw.1.zip	Raw
	E-GEOD-17365.sdrf.txt	Txt

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Publications

Caspase-8 deficiency in epidermal keratinocytes triggers an inflammatory skin disease.

Kovalenko Andrew A Kim Jin-Chul JC Kang Tae-Bong TB Rajput Akhil A Bogdanov Konstantin K Dittrich-Breiholz Oliver O Kracht Michael M Brenner Ori O Wallach David D

The Journal of experimental medicine 20090831 10

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 nuclear factor kappaB activation in the epidermal cells, the effect induced by caspase-8 deficiency did not depend on TNF, IL-1, 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 ...[more]

PMID: 19720838

Similar Datasets

Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

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

| E-GEOD-17365 | BioStudies

Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

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/–K5-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 | ArrayExpress

Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice

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 | ArrayExpress

Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice

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).

| E-GEOD-17344 | BioStudies

Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/M-bM-^@M-^SK5-Cre and Casp-8F/+K5-Cre mice

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).

| E-GEOD-17345 | BioStudies

Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice

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. Overall design: 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 | GSE17344 | GEO

Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

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. Overall design: Epidermal keratinocytes were isolated from the skin of Casp-8F/–K5-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 | GSE17345 | GEO

Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

Project description:Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

| PRJNA119089 | ENA

Mus musculus

Project description:Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

| PRJNA123609 | ENA

Mus musculus

Project description:Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice

| PRJNA123607 | ENA