Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA123609 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice
| PRJNA119089 | ENA
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:Rac signaling affects numerous downstream targets; however, few studies have established in vivo levels using model animals. In the present study, wWe generated mice with a single knockout (KO) of Rac1 (Keratin5 (K5)-Cre;Rac1flox/flox, hereafter Rac1-KO) and double KO of Rac1 and Rac3 (K5-Cre;Rac1flox/flox;Rac3−/−, hereafter Rac1/Rac3-DKO) in keratinocytes. Hairless phenotype in Rac1-KO mice was markedly exacerbated in Rac1/Rac3-DKO mice. Notably, Rac1-KO mice also exhibited thinner dermal white adipose tissue, which was considerably further reduced in Rac1/Rac3-DKO mice. DNA microarray using primary keratinocytes from Rac1/Rac3-DKO mice exhibited decreased mRNA levels of Bmp2, Bmp5, Fgf20, Fgf21, Fgfbp1, and Pdgf-alpha. Combinational treatment with BMP2 and FGF21, BMP2 and FGF20, or PDGF and FGF21 in culture medium, but not individual purified recombinant proteins, could differentiate 3T3-L1 fibroblasts into adipocytes, as could culture media obtained from primary keratinocytes (both human and mouse). Conversely, addition of anti-BMP2 or anti-FGF21 antibodies into the culture medium inhibited fibroblast differentiation. Furthermore, combinational treatment with BMP2 and FGF21 promoted adipocyte differentiation only of rat primary white adipocyte precursors but not rat primary brown adipocyte precursors. Notably, brown adipogenesis by FGF21 was inhibited by BMP2. Thus, we here proposed a novel paracrine pathway from keratinocytes to intradermal pre-adipocytes using Rac1/Rac3-DKO mice, which is Rac-dependent and functions as an inducer of white adipocytes.
2019-11-06 | GSE122234 | GEO
Project description:We performed microarray analysis to examine the differential gene expression profiles between Prdm1 (Blimp-1)-deleted and control keratinocytes. Keratinocytes isolated from Prdm1-floxed K5-CreER positive (CKO) mice were cultured in the presence of 4OHT to induce deletion of the Prdm1 allele in vitro. Prdm1-floxed K5-CreER positive (CKO) keratinocytes treated with the ethanol solvent control (EtOH) or Prdm1-floxed K5-CreER negative (control) keratinocytes treated with 4OHT or EtOH served as controls. Microarray analyses revealed that there were 93 genes up-regulated and 109 genes down-regulated by more than 2-fold in the CKO + 4OHT group in comparison with the CKO + EtOH, Ctrl + 4OHT or Ctrl + EtOH groups. Several corneocytes-related genes, including Rptn, Lce1f, Krt1 and Lce1d, are significantly down-regulated and several cytokines/chemokines, including Cxcl1, Cxcl2, Cxcl5 and Il24, are significantly up-regulated upon the deletion of Prdm1 in vitro.
2013-04-02 | GSE34586 | GEO
Project description:We performed microarray analysis to examine the differential gene expression profiles between Prdm1 (Blimp-1)-deleted and control keratinocytes. Keratinocytes isolated from Prdm1-floxed K5-CreER positive (CKO) mice were cultured in the presence of 4OHT to induce deletion of the Prdm1 allele in vitro. Prdm1-floxed K5-CreER positive (CKO) keratinocytes treated with the ethanol solvent control (EtOH) or Prdm1-floxed K5-CreER negative (control) keratinocytes treated with 4OHT or EtOH served as controls. Microarray analyses revealed that there were 93 genes up-regulated and 109 genes down-regulated by more than 2-fold in the CKO + 4OHT group in comparison with the CKO + EtOH, Ctrl + 4OHT or Ctrl + EtOH groups. Several corneocytes-related genes, including Rptn, Lce1f, Krt1 and Lce1d, are significantly down-regulated and several cytokines/chemokines, including Cxcl1, Cxcl2, Cxcl5 and Il24, are significantly up-regulated upon the deletion of Prdm1 in vitro. We analyzed the transcription profiles in control and Blimp-1-deficient keratinocytes using the GeneChip® Mouse Expression Array 430A.
2013-04-02 | E-GEOD-34586 | 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
Project description:RNA-seq of keratinocytes derived from Pp6fl/fl and K5.Pp6fl/fl mice
2018-11-20 | GSE122665 | GEO