LncRNA H19X was silienced in dermal fibroblats of systemic sclerosis patients with antisense oligonuclotides. The hypothesis tested in the present study was that H19X is an important factor in the development of TGFb-driven fibrosis. Results provide important information about the role H19X in fibroblasts in particolar on extracellular matrix production and cell cycle regulation.
Long noncoding RNA H19X is a key mediator of TGF-β-driven fibrosis.
Specimen part, Disease, Disease stage, Treatment
View SamplesWe generated mice with a transgenic BAC on a B6 background. The BAC contains Glo1, and the transgenic mice were found to overexpress Glo1.
Glyoxalase 1 increases anxiety by reducing GABAA receptor agonist methylglyoxal.
Sex, Specimen part
View SamplesComparative analysis of gene expression profiles in newly developed housing systems is important to understand gene functions in chicken for adaptation and possible gene-environment interactions among layer lines. Therefore, the objective of this study was to characterize the molecular processes that are different among the two layer lines Lohmann Selected Leghorn (LSL) and Lohmann Brown (LB) using whole genome RNA expression profiles. Despite their approximately identical egg production performance these layer lines differ markedly in other phenotypic traits. The two layer lines were kept under the production environment of the newly developed small group housing system Eurovent German with two different group sizes and three tiers.
Differential gene expression from genome-wide microarray analyses distinguishes Lohmann Selected Leghorn and Lohmann Brown layers.
Specimen part
View SamplesTo address the functional role of KDM6A in the regulation of Rhox genes, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Kdm6a mRNA. We found that Kdm6a knockdown in mouse ES cells caused a decrease in expression of a subset of Rhox genes, Rhox6 and 9. Furthermore, Rhox6 and 9 expression was decreased in female ES cells but not male ES cells indicating that KDM6A regulates Rhox gene expression in a sexually dimorphic manner.
Female bias in Rhox6 and 9 regulation by the histone demethylase KDM6A.
Specimen part, Cell line
View SamplesTo address the functional role of MOF in mammalian X upregulation, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Mof mRNA. We found that MOF knockdown in mouse ES cells caused a greater drop in expression of X-linked genes compared to autosomal genes, as measured by expression array analyses. The strongest effect was observed on medium-expressed X-linked genes.
Mammalian X upregulation is associated with enhanced transcription initiation, RNA half-life, and MOF-mediated H4K16 acetylation.
Specimen part, Treatment
View SamplesDosage compensation restores a balanced network of gene expression between autosomes and sex chromosomes in males (XY) and females (XX). In mammals, this is achieved by doubling the expression of X-linked genes in both sexes, together with X inactivation in females. X up-regulation may be controlled by DNA sequence based and/or epigenetic mechanisms that double the X output potentially in response to an autosomal counting factor. Human triploids with either one or two active X chromosomes (Xa) provide a mean to test X chromosome expression in the presence of three sets of autosomes, which will help understand the underlying mechanisms of X up-regulation.
Dosage regulation of the active X chromosome in human triploid cells.
Sex, Specimen part
View SamplesAffymetrix 430 2.0 mouse arrays were used for expression analyses in undifferentiated and differentiated PGK12.1 ES cells. We found that the X:autosome expression ratios calculated from the mean expression values of X-linked and autosomal genes from microarrays was ~1.4 in undifferentiated female ES cells and then decreased to 1.2 in PGK12.1 cells after 15-day embryoid body differentiation. Thus, a substantial level of X upregulation is already evident in these ES cells prior to differentiation.
Mammalian X upregulation is associated with enhanced transcription initiation, RNA half-life, and MOF-mediated H4K16 acetylation.
Specimen part
View SamplesRNA-Seq was used to profile transcriptional changes induced by overexpression of the long non-coding RNA SLNCR1, as well as mutant version SLNCR1 delta conserved and SLNCR1 conserved. Overall design: The A375 melanoma cell line was transfected with pcDNA3.1 (-) expressing either full length SLNCR1, SLNCR1 delta conserved, or SLNCR1 conserved.
The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
No sample metadata fields
View SamplesRNA-Seq was used to profile transcriptional changes induced by siRNA knockdown of the long non-coding RNA SLNCR1. Overall design: The WM1976 melanoma short-term culture was transfected with either scrambled or SLNCR1-targeting siRNAs
The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
No sample metadata fields
View SamplesThe CCCTC-binding factor (CTCF) is a versatile transcriptional regulator required for embryogenesis, but its function in vascular development or in diseases with a vascular component is poorly understood. Here, we found that endothelial Ctcf is essential for mouse vascular development and limits accumulation of reactive oxygen species (ROS). Conditional knockout of Ctcf in endothelial progenitors and their descendants affected embryonic growth, and caused lethality at embryonic day 10.5 owing to defective yolk sac and placental vascular development. Analysis of global gene expression revealed Frataxin (Fxn), the gene mutated in Friedreich's ataxia (FRDA), as the most strongly downregulated gene in Ctcfdeficient placental endothelial cells. Moreover, in vitro reporter assays showed that Ctcf activates the Fxn promoter in endothelial cells. Reactive oxygen species (ROS) are known to accumulate in the endothelium of FRDA patients. Importantly, Ctcf deficiency induced ROS-mediated DNA damage in endothelial cells in vitro, and in placental endothelium in vivo. Taken together, our findings indicate that, Ctcf promotes vascular development, and limits oxidative stress in endothelial cells, perhaps through activation of Fxn transcription. These results reveal a function for a Ctcf–Fxn transcriptional pathway in vascular development, and also suggest a potential mechanism for endothelial dysfunction in FRDA. Overall design: Examination of transcriptome profiles of placental endothelial cells isolated from wildtype or ctcf defecient endothelial cells at E9.5
The transcriptional regulator CCCTC-binding factor limits oxidative stress in endothelial cells.
Specimen part, Subject
View Samples