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accession-icon GSE146109
VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment

View Samples
accession-icon GSE146108
VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [HBMEC]
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.

Publication Title

VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE146107
VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [mouse heart]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.

Publication Title

VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE74034
Estrogen receptor promotes breast cancer by reprogramming cell metabolism
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st), Illumina Genome Analyzer

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Estrogen Receptor α Promotes Breast Cancer by Reprogramming Choline Metabolism.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE74032
Estrogen receptor promotes breast cancer by reprogramming cell metabolism [gene expression]
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Estrogen receptor (ER) is a key regulator of breast growth and breast cancer development. However, the role of ER in metabolic reprogramming, a hallmark of cancer, is not well documented. In this study, using an integrated approach combining genome-wide mapping of chromatin bound ER with estrogen induced transcript and metabolic profiling, we demonstrate that ER reprograms metabolism upon estrogen stimulation, including changes in aerobic glycolysis, nucleotide and amino acid synthesis, and choline metabolism. We show, for the first time, that the ER target gene choline phosphotransferase 1 (CHPT1) plays an essential role in estrogen induced increases in phosphatidylcholine (PtdCho) levels and that CHPT1 promotes tumorigenesis and proliferation. Furthermore, we show that CHPT1 is overexpressed in tumors compared to normal breast. We also demonstrate that ER promotes aerobic glycolysis through increased expression of glycolytic genes. In conclusion, this study highlights the importance of ER for metabolic alterations in breast cancer cells. Furthermore, overexpression of the ER target CHPT1 in breast cancer supports its potential as a therapeutic target.

Publication Title

Estrogen Receptor α Promotes Breast Cancer by Reprogramming Choline Metabolism.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE28976
Expression data from human breast cancer cell lines after demethylation treatment
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrated epigenetics of human breast cancer: synoptic investigation of targeted genes, microRNAs and proteins upon demethylation treatment.

Sample Metadata Fields

Treatment

View Samples
accession-icon GSE28968
MRNA expression data from human breast cancer cell lines after demethylation treatment.
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The contribution of aberrant DNA methylation and the downstream effects in tumorogenesis through silencing of tumor suppressor genes (TSGs) and microRNAs has been investigated. Since these epigenetic alterations can be reversed, we investigated the effects of the epigenetic therapy in breast cancer cell lines.

Publication Title

Integrated epigenetics of human breast cancer: synoptic investigation of targeted genes, microRNAs and proteins upon demethylation treatment.

Sample Metadata Fields

Treatment

View Samples
accession-icon GSE31080
Effect of interleukin-1 and PDGF-DD on SMCs
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This experiment tests the hypothesis that interleukin-1 promotes SMC phenotypic modulation to a distinct inflammatory state relative to the growth factor PDGF-DD.

Publication Title

Interleukin-1β modulates smooth muscle cell phenotype to a distinct inflammatory state relative to PDGF-DD via NF-κB-dependent mechanisms.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP021210
Danio rerio strain:Wildtype strains AB, WIK, and AB/Tueb Transcriptome or Gene expression
  • organism-icon Danio rerio
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaHiSeq2000

Description

Gene expression profiling of several wildtype strains of zebrafish embryos. The samples were pooled from several developmental stages ranging from 2 to 7 days post fertilization. This breadth of sampling gives a broad idea of genes expressed during early development and SNPs associated with wildtype strains.

Publication Title

RNA-seq-based mapping and candidate identification of mutations from forward genetic screens.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP061252
Minocycline counter regulates the global pro-inflammatory response in microglia and protects from retinal degeneration
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Minocycline is a potent modulator of retinal microglia Overall design: Global mRNA expression analysis of CD1 mouse retinas in control, light damage and light damage plus minocycline conditions

Publication Title

Minocycline counter-regulates pro-inflammatory microglia responses in the retina and protects from degeneration.

Sample Metadata Fields

No sample metadata fields

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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Developed by the Childhood Cancer Data Lab

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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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