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.
No associated publication
Sex, Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.
Age, Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.
Specimen part, Treatment
View SamplesEndothelial 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.
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.
Age, Cell line, Treatment
View SamplesImpaired 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.
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.
No sample metadata fields
View SamplesImpaired 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.
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.
No sample metadata fields
View SamplesTranscriptional profiling of ErbB4-/- mouse liver tissues comparing controls.
ERBB4 acts as a suppressor in the development of hepatocellular carcinoma.
Specimen part, Treatment
View SamplesThis study aims to compare mRNA expression between radiated and non-radiated human keratinocyte HaCaT cells by microarray analysis. Human keratinocyte HaCaT cells were divided into two groups, each group has three repeats. The cells were irradiated with a single dose of 0 or 20Gy of X-ray irradiation. 48 hours post radiation, cells from 0 or 20 Gy groups were collected and subjected to microarray analysis.
No associated publication
Specimen part, Cell line, Treatment
View SamplesAnalysis of the effects of the rs4919510C>G SNP on miRNA-608 target gene expression. The hypothesis tested in the present study was that the rs4919510C>G SNP may influence the expression of miRNA-608 target genes. Results provide important information of the effects of the rs4919510C>G SNP on miRNA-608 target genes, including immunity and defense genes, DNA repair genes, cell growth-related genes, tumor invasion and metastasis-related genes, cancer stem cell-related genes, and cell death-related genes.
No associated publication
Specimen part, Cell line
View SamplesCells 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.
In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes.
Specimen part
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