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GSE62648
Mus musculus
8 Downloadable Samples
Description
Dietary collagen hydrolysate has been conjectured to improve skin barrier function. To investigate the effect of long-term collagen hydrolysate administration on the skin, we evaluated stratum corneum water content and skin elasticity in intrinsic aged mice. Female 9-week-old hairless mice were fed a control diet, or a collagen hydrolysate-containing diet, for 12 weeks. The stratum corneum water content and skin elasticity were sequentially decreased by chronological aging in control mice. Intake of collagen hydrolysate significantly suppressed such changes. Moreover, we comprehensively analyzed gene expression in the skin of mouse, which had been administered collagen hydrolysate, using DNA microarray. Twelve weeks after start of collagen intake, no significant differences appeared in gene expression profile compared to that of control group. However, 1 week after administration, 135 genes were up-regulated and 448 genes were down-regulated in collagen group compared to control group. It is indicate that gene changes preceded changes of barrier function and elasticity. We focused on several genes correlated with functional changes in the skin. Gene Ontology terms, especially related to epidermal cell development, were signicantly enriched in up-regulated genes. These skin function-related genes had properties that facilitate epidermal production and differentiation and suppress dermal degradation. Thus, dietary collagen hydrolysate induced positive gene changes. In conclusion, our results suggest that alteration of gene expression at early stages after collagen administration affect skin barrier function and mechanical properties. Long-term oral intake of collagen hydrolysate improves skin dysfunction by regulating genes related to production and maintenance of the skin tissue.
Publication Title
Effect of orally administered collagen hydrolysate on gene expression profiles in mouse skin: a DNA microarray analysis.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
Description
To identify the target genes of Evi-1 in hematopoietic stem cells (HSCs), we carried out genome-wide transcriptional analysis using wild-type and Evi-1-deleted HSCs.
Publication Title
Evi-1 is a critical regulator for hematopoietic stem cells and transformed leukemic cells.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 6 Downloadable Samples
Description
To clarify inflammatory genes whose expression is suppressed at high temperatures, we performed comprehensive analysis of gene expression by using a DNA microarray. Two independent primary cultures of mouse embryo fibroblasts (MEF1 and MEF2) were treated with LPS for 4 hours, or treated with LPS for 4 hours after the pretreatment with heat shock at 42C for 1 hour, and we identified 100 genes that undergo more than a 3-fold increase with LPS treatment. Remarkably, 86 genes (86%) underwent less than a 2-fold increase after combined treatments with heat shock and LPS in MEF1 and MEF2 cells.
Publication Title
Heat shock transcription factor 1 inhibits expression of IL-6 through activating transcription factor 3.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Forced expression of the histone demethylase Fbxl10 maintains self-renewing hematopoietic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Mouse CD34(-)KSL hematopoietic stem cells and CD34(+)KSL multipotent progenitors were purified by cell sorting from bone marrow of 8-week-old C57BL/6 mice, and their gene expression was analyzed.
Publication Title
Forced expression of the histone demethylase Fbxl10 maintains self-renewing hematopoietic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
Histone H3 lysine 9 (H3K9) methylation is an epigenetic mark of transcriptionally repressed chromatin. During mammalian development, H3K9 methylation levels seem to be spatiotemporally regulated by the opposing activities of methyltransferases and demethylases to govern correct gene expression. However, the combination(s) of H3K9 methyltransferase(s) and demethylase(s) that contribute to this regulation and the genes regulated by them remain unclear. Herein, we demonstrate the essential roles of H3K9 demethylases Jmjd1a and Jmjd1b in the embryogenesis and viability control of embryonic stem (ES) cells. Mouse embryos lacking Jmjd1a/Jmjd1b died after implantation. Depletion of Jmjd1a/Jmjd1b in mouse ES cells induced rapid cell death accompanied with a massive increase in H3K9 methylation. Jmjd1a/Jmjd1b depletion induced an increase in H3K9 methylation in the gene-rich regions of the chromosomes, indicating that Jmjd1a/Jmjd1b removes H3K9 methylation marks in the euchromatin. Importantly, the additional disruption of the H3K9 methyltransferase G9a in a Jmjd1a/Jmjd1b-deficient background rescued not only the H3K9 hypermethylation phenotype but also the cell death phenotype. We also found that Jmjd1a/Jmjd1b removes H3K9 methylation marks deposited by G9a in the Oct4 and Ccnd1 loci to activate transcription. In conclusion, Jmjd1a/Jmjd1b ensures ES cell viability by antagonizing G9a-mediated H3K9 hypermethylation in the gene-rich euchromatin.
Publication Title
Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis.
Sample Metadata Fields
Specimen part
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