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Mus musculus
2 Downloadable Samples
Illumina HiSeq 2000
Description
The project investigated the role of Leucine-rich a2-glycoprotein 1 (LRG1) in the vascularization, immunogenicity and growth of B16F0 subcutaneous tumours in Control and LRG1 global knock out mice.
Publication Title
No associated publication
Alternate Accession IDs
None
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Cell line
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
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.
Alternate Accession IDs
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment
View Samples
GSE107033- Homo sapiens
- 11 Downloadable Samples
- 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.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
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.
Alternate Accession IDs
Sample Metadata Fields
Age, Cell line, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- 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.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- 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.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- 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.
Alternate Accession IDs
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The adipose tissue is an endocrine regulator and a risk factor for atherosclerosis and cardiovascular disease when by excessive accumulation induces obesity. Although the adipose tissue is also a reservoir for stem cells (ASC) their function and stemcellness has been questioned. Our aim was to investigate the mechanisms by which obesity affects subcutaneous white adipose tissue (WAT) stem cells.
Publication Title
Stem cells isolated from adipose tissue of obese patients show changes in their transcriptomic profile that indicate loss in stemcellness and increased commitment to an adipocyte-like phenotype.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Bos indicus, Bos taurus
- 26 Downloadable Samples
- Affymetrix Bovine Genome Array (bovine)
Description
We examined gene expression induced by Rhipicephalus microplus bites on host skin of tick-resistant and tick-susceptible breeds of bovines, Nelore and Holstein respectively, when they underwent a primary infestation.
Publication Title
Immune and biochemical responses in skin differ between bovine hosts genetically susceptible and resistant to the cattle tick Rhipicephalus microplus.
Alternate Accession IDs
None
Sample Metadata Fields
Sex, Specimen part, Subject, Time
View Samples- Mus musculus, Homo sapiens
- 37 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Cells were reprogrammed from cardiac fibroblasts to cardiomyocytes, in various conditions. These are the iCM cells (induced cardiomyocytes). There are both human and mouse arrays here, as seen below.
Publication Title
In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
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