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accession-icon GSE143151
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment

View Samples
accession-icon GSE107033
Endothelial gene expression analysis
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE143150
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition [microarray]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Human Exon 1.0 ST Array (huex10st)

Description

Endothelial cells play an important role in maintenance of the vascular system and the repair after injury. Under pro-inflammatory conditions, endothelial cells can acquire a mesenchymal phenotype by a process named endothelial-to-mesenchymal transition (EndMT), which affects the functional properties of endothelial cells. Here, we investigated the epigenetic control of EndMT. We show that the histone demethylase JMJD2B is induced by EndMT promoting pro-inflammatory and hypoxic conditions. Silencing of JMJD2B reduced TGF-β2-induced expression of mesenchymal genes and prevented the alterations in endothelial morphology and impaired endothelial barrier function. Endothelial-specific deletion of JMJD2B in vivo confirmed a reduction of EndMT after myocardial infarction. EndMT did not affect global H3K9me3 levels but induced a site-specific reduction of repressive H3K9me3 marks at promoters of mesenchymal genes, such as Calponin (CNN1), and genes involved in TGF-β signaling, such as AKT Serine/Threonine Kinase 3 (AKT3) and sulfatase 1 (SULF1). Silencing of JMJD2B prevented the EndMT-induced reduction of H3K9me3 marks at these promotors and further repressed these EndMT-related genes. Our study reveals that endothelial identity and function is critically controlled by the histone demethylase JMJD2B, which is induced by EndMT-promoting pro-inflammatory and hypoxic conditions and support the acquirement of a mesenchymal phenotype.

Publication Title

The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.

Sample Metadata Fields

Age, Cell line, Treatment

View Samples
accession-icon GSE107032
Endothelial gene expression analysis after silencing LOXL2 using siRNAs
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulates endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is up-regulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-2-induced endothelial-mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.

Publication Title

The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE107031
Endothelial gene expression analysis after silencing the lncRNA GATA6-AS using LNA GapmeRs.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulates endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is up-regulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-2-induced endothelial-mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.

Publication Title

The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE68619
Expression data from bone marrow cells of type 2 diabetic mice and wild type mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

More and more studies pointed out that BM was the primary target of diabetes mellitus-induced damage. The aim of this study was to determine whether distinct gene expression profiles are associated with altered functions of bone marrow cells in diabetes mellitus type 2 mice.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE27975
HL-1 cardiomyocyte response to hypoxia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.

Publication Title

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP095659
Mus musculus Raw sequence reads
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2500

Description

We investigate the molecular mechanisms of the RP9 mutation causing photoreceptor degeneration using the 661w cell

Publication Title

Targeted RP9 ablation and mutagenesis in mouse photoreceptor cells by CRISPR-Cas9.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP095666
Mus musculus Raw sequence reads
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2500

Description

RP9 point mutation of 661w cell

Publication Title

Targeted RP9 ablation and mutagenesis in mouse photoreceptor cells by CRISPR-Cas9.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP095667
Mus musculus Raw sequence reads
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2500

Description

RP9 konck out of 661w cell

Publication Title

Targeted RP9 ablation and mutagenesis in mouse photoreceptor cells by CRISPR-Cas9.

Sample Metadata Fields

Sex, Specimen part

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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