Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA270895 | ENA |
REPOSITORIES: ENA
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Project description:Comparative analysis of gene expression in cultured primary keratinocytes isolated from newborn control (K14-cre; GPx4fl/+) and knockout (K14-cre; GPx4fl/fl) mice. Selenoproteins are essential for skin function, as targeted abolition of selenoproteins in epidermal tissue results in newborn mice manifesting gross abnormalities of skin and hair, accompanied by retarded growth and premature death. To investigate whether lack of a single selenoprotein could induce similar phenotypic effect in mice, we generated keratinocyte-specific knockout mice lacking glutathione peroxidase 4 (GPx4), an essential selenoprotein in skin, to examine phenotypic changes resulting from the lack of GPx4 in skin. Ablation of GPx4 results in focal alopecia and disturbed hair follicle morphogenesis, with GPx4 being essential during early stages of hair follicle morphogenesis as well as for keratinocyte adhesion and proliferation in culture. We have generated mice with selective removal of the GPx4 gene in keratinocytes under the control of Keratin-14-cre (K14-cre) promoter. Comparative microarray analysis was performed on RNA samples taken from pooled primary keratinocytes from knockout and control mice from the same litter. Array replicates were performed using RNA samples from three different litters.
2012-12-06 | E-GEOD-34215 | biostudies-arrayexpress
Project description:RABGEF1, a guanine nucleotide exchange factor for Rab5 GTPase, can negatively regulate mast cell activation in vitro. In addition, RabGEF1-deficient mice develop morbidity and severe skin inflammation associated with marked increases in skin mast cell numbers (Tam et al., Nat Immunol, 5(8):844-52, 2004). These findings suggest that over-reactive skin mast cells may contribute to the observed skin pathology in vivo. In order to identify the cell type(s) which contribute to skin inflammation when RabGEF1 is absent, we attempted to delete Rabgef1 gene specifically in three major skin cell types, namely mast cells, myeloid cells and keratinocytes; thus, Rabgef1 floxed (fl/fl) mice were crossed with mice expressing the Cre-recombinase under the influence of the promoter of Mcpt5, LysZ or K14, respectively. Unexpectedly, Mcpt5-Cre;Rabgef1fl/fl and Lysz-Cre;Rabgef1fl/fl mice appeared normal without phenotypic abnormalities. However, K14-Cre;Rabgef1fl/fl mice were normal at birth but rapidly developed morbidity and skin inflammation after 2-3 days, and died between 1 and 8 weeks of age. Skin (epidermis + dermis) was sampled from the center of the back behind shoulders, for 2 conditional knock-out mice (Rabgef1 lox/lox K14-Cre, hereafter called Rabgef1K-KO) and 2 control mice (Rabgef1 lox/lox). Total RNA was isolated from mouse skin using Trizol. Gene expression analysis was performed using Affymetrix Mouse Genome 430 2.0 arrays, with two replicates per genotype. Microarray data were analysed using Bioconductor for R.
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Project description:Engrams are considered to be substrates for memory storage, and the functional dysregulation of the engrams leads to cognition impairment.However, the cellular basis for these maladaptive changes lead to the forgetting of memories remains unclear. Here we found that the expression of autophagy protein 7 (Atg7) mRNA was dramatically upregulated in aged DG engrams, and led to the forgetting of contextual fear memory and the activation of surrounding microglia.To determine mechanism by which autophagy in DG engrams activates the surrounding microglia, mice were co-injected AAV-RAM-Cre either with AAV-Dio-Atg7-Flag or AAV-Dio- EYFP in dorsal dentate gyrus to overexpress ATG7 in the DG memory engrams. Microglia were separated using magnetic-activated cell sorting and subjected to RNA-Seq in dorsal hippocampus .Bioinformatics analysis shown overexpression of Atg7 in dorsal DG memory engrams caused an increase in the expression of Tlr2 in the surrounding microglia.Depletion of Toll-like receptor 2/4 (TLR2/4) in DG microglia prohibited excessive microglial activation and synapse elimination induced by the overexpression of ATG7 in DG engrams, and thus prevented forgetting. Furthermore, the expression of Rac1, a Rho-GTPases which regulates active forgetting in both fly and mice, was upregulated in aged engrams. Optogentic activation of Rac1 in DG engrams promoted the autophagy of the engrams, the activation of microglia, and the forgetting of fear memory. Invention of the Atg7 expression and microglia activation attenuated forgetting induced by activation of Rac1 in DG engrams. Together, our findings revealed autophagy-dependent synapse elimination of DG engrams by microglia as a novel forgetting mechanism.
2021-08-24 | GSE169019 | GEO
Project description:Comparative analysis of gene expression in cultured primary keratinocytes isolated from newborn control (K14-cre; GPx4fl/+) and knockout (K14-cre; GPx4fl/fl) mice. Selenoproteins are essential for skin function, as targeted abolition of selenoproteins in epidermal tissue results in newborn mice manifesting gross abnormalities of skin and hair, accompanied by retarded growth and premature death. To investigate whether lack of a single selenoprotein could induce similar phenotypic effect in mice, we generated keratinocyte-specific knockout mice lacking glutathione peroxidase 4 (GPx4), an essential selenoprotein in skin, to examine phenotypic changes resulting from the lack of GPx4 in skin. Ablation of GPx4 results in focal alopecia and disturbed hair follicle morphogenesis, with GPx4 being essential during early stages of hair follicle morphogenesis as well as for keratinocyte adhesion and proliferation in culture.
2012-12-06 | GSE34215 | GEO
Project description:mRNA expression profile for skin tissues from 3-days-old wildtype and RNF31fl/fl-K14-cre mice.
2019-06-08 | GSE111297 | GEO