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accession-icon GSE62650
Gene expression profiles in dorsal skin of hairless mice orally administrated collagen hydrolysate
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

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
accession-icon GSE62649
Gene expression profiles in dorsal skin of hairless mice orally administrated collagen hydrolysate for 12 weeks
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

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, 12 weeks 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
accession-icon GSE62648
Gene expression profiles in dorsal skin of hairless mice orally administrated collagen hydrolysate for 1 week
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

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
accession-icon GSE49486
Effect of ingested whey protein hydrolysate on gene expression profiles compared to an identical composition of amino acid mixture in rat skeletal muscle
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

We have previously showed that whey protein hydrolysate (WPH) causes a greater increase in muscle protein synthesis than an identical composition of amino acids mixture does. The present study was conducted to investigate a comparative effect of WPH on gene expression. Male Sprague-Dawley rats subjected to a 2-h swimming exercise were administered either a carbohydrate-amino acid diet or a carbohydrate-WPH diet immediately after exercise. One hour after exercise, epitrochlearis muscle mRNA was sampled and subjected to DNA microarray analysis. As a result, ingestion of WPH altered 189 genes in considering the false discovery rate. Among the upregulated genes, 8 Gene Ontology (GO) terms were enriched, which included key elements in muscle repair after exercise such as Cd24, Ccl2, Ccl7 and Cxcl1. On the other hand, 9 GO terms were enriched in the gene sets downregulated by ingestion of WPH and these GO terms fell into 2 clusters, regulation of ATPase activity, and immune response. Furthermore, we found that WPH activate the 2 upstream proteins, extracellular signal-regulated kinase 1/2 (ERK1/2) and hypoxia-inducible factor-1 (HIF-1), which may act as key factors for regulation of gene expression. These results suggest that ingestion of WPH, compared to an identical composition of amino acid mixture, induces greater changes in the after-exercise gene expression profile via activation of the proteins, ERK1/2 and HIF-1.

Publication Title

Post-exercise impact of ingested whey protein hydrolysate on gene expression profiles in rat skeletal muscle: activation of extracellular signal-regulated kinase 1/2 and hypoxia-inducible factor-1α.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon GSE103459
Expression date from WT RAW264.7 and HuR-deficient RAW264.7 stimulated with poly(I:C) using lipofectamine
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

HuR-deficient cells showed the decreased expression of genes involved in chemotaxis, cell proliferation and signal transduction.

Publication Title

Hu Antigen R Regulates Antiviral Innate Immune Responses through the Stabilization of mRNA for Polo-like Kinase 2.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE25029
Ionizing radiation in GI tract of Tweak KO mice
  • organism-icon Mus musculus
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

TWEAK/Fn14 signaling may regulate the expression of genes involved in epithelial repair and mucosal inflammation. Comparing the gene signatures in WT and TWEAK KO mice will inform the biology of TWEAK/Fn14 pathway in the GI tract.

Publication Title

Interleukin-13 damages intestinal mucosa via TWEAK and Fn14 in mice-a pathway associated with ulcerative colitis.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE28641
Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Dynamic chromatin localization of Sirt6 shapes stress- and aging-related transcriptional networks.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE28585
Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks (Illumina)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Sirtuins (Sirt) are a family of enzymes that modify chromatin and other proteins to affect gene activity. Loss of Sirt6 leads to a progeria-like phenotype in mice, but the target of SIRT6 action has been elusive. Here we show that Sirt6 binds to thousands of gene promoters in a stress-inducible fashion, guided by the stress-responsive transcription factor NF-B.

Publication Title

Dynamic chromatin localization of Sirt6 shapes stress- and aging-related transcriptional networks.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP033291
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq1000

Description

Superior frontal gyrus grey and white matter

Publication Title

Unique transcriptome patterns of the white and grey matter corroborate structural and functional heterogeneity in the human frontal lobe.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP102352
TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Atopic dermatitis and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. We show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of atopic dermatitis-specific Th2 and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in atopic dermatitis, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naïve mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis. Overall design: Eight- to 12-week old male mice were used. TWEAK-deficient animals were bred in house on the C57BL/6 background, and Fn14-deficient animals on a BALB/c. Atopic Dermatitis-like disease was induced by epicutaneous treatment with HDM extract (10 µg/mouse and treatment) and SEB (500 ng/mouse and treatment) given in 2 cycles on days 1 and 4, and 14 and 17, on the shaved and tape-stripped back skin over a 23 day period.

Publication Title

TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.

Sample Metadata Fields

Treatment, Subject

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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