Fine needle stimulation also known as acupuncture is a traditional Chinese medical practice which causes relief of pain. We demonstrated that it caused neovascularization and enhanced recovery of blood perfusion in a ischemic portion of skeletal muscle in rats with hindlimb ischemia. Therefore we evaluated the effect of fine needle stimulation on skeletal muscle at gene expression level
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View SamplesDiscarded human aortic valve samples from the second trimester, six from early (14, 15, 17 weeks), and six from late timepoints (20, 21, 22 weeks) were collected. RNA was isolated and cDNA libraries were sequenced. Network analysis of RNASeq data identified subnetworks of significantly increasing and decreasing transcripts; subsequent cluster analysis identified patterns of transcription through the time course. Pathway enrichment analysis determined the predominant biological processes at each interval.
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Sex, Specimen part
View SamplesThe 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.
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.
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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 SamplesGastric cancers account for the fourth most frequent cancer death worldwide. Although many differential gene expression profiles are reported for gastric cancers, their variation at the post-transcriptional level has not been provided yet. In this study, we compared the gene expressions of normal stomach vs. stomach cancer in an exon-wise manner and compared alternatively spliced transcripts. The RNA from normal and cancer tissues of gastric cancer patients were subjected to Exon 1.0 ST microarrays.
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Sex, Specimen part, Subject
View SamplesTo compare the gene expression profile of MSCs harvested from bone marrow in the context of cell migration.
Matrix metalloproteinase 1 is necessary for the migration of human bone marrow-derived mesenchymal stem cells toward human glioma.
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