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Rattus norvegicus
9 Downloadable Samples
Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
We demonstrated that, four weeks after the pulmonary artery banding (PAB) operation, rats could be divided into two groups: an F+ group in which the fibrotic area occupied more than 6.5% of the whole area of the heart tissues, and an F- group in which the fibrotic area occupied less than 6.5% of this area.
Publication Title
Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1.
Sample Metadata Fields
Sex, Specimen part
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Endothelial cells (Ecs) lining the blood vessels have been known to have a variety of functions and play a central role in homeostasis of the circulatory system.
Publication Title
Transcription profiles of endothelial cells in the rat ductus arteriosus during a perinatal period.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 2 Downloadable Samples
- Affymetrix Rat Genome U34 Array (rgu34a)
Description
To identify a novel target for the treatment of heart failure, we examined gene expression in the failing heart. Among the genes analyzed, 12/15 lipoxygenase (12/15-LOX) was markedly up-regulated in heart failure. To determine whether increased expression of 12/15-LOX causes heart failure, we established transgenic mice that overexpressed 12/15-LOX in cardiomyocytes. Echocardiography showed that 12/15-LOX transgenic mice developed systolic dysfunction. Cardiac fibrosis increased in 12/15-LOX transgenic mice with advancing age, and was associated with the infiltration of macrophages. Consistent with these observations, cardiac expression of monocyte chemoattractant protein-1 (Mcp-1) was up-regulated in 12/15-LOX transgenic mice compared with wild-type mice. Treatment with 12-hydroxy-eicosatetraenotic acid, a major metabolite of 12/15-LOX, increased MCP-1 expression in cardiac fibroblasts and endothelial cells, but not in cardiomyocytes. Inhibition of Mcp-1 reduced the infiltration of macrophages into the myocardium and prevented both systolic dysfunction and cardiac fibrosis in 12/15-LOX transgenic mice. Likewise, disruption of 12/15-LOX significantly reduced cardiac Mcp-1 expression and macrophage infiltration, thereby improving systolic dysfunction induced by chronic pressure overload. Our results suggest that cardiac 12/15-LOX is involved in the development of heart failure and that inhibition of 12/15-LOX could be a novel treatment for this condition.
Publication Title
Cardiac 12/15 lipoxygenase-induced inflammation is involved in heart failure.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of umbilical vein endothelial cells (HUVEC) treated with Egr-3 siRNA under the VEGF treatment for 0,1, and 4 h. Egr-3, a member of early growth response family, is immediately and dramatically induced by VEGF in HUVEC, which regulates expression of many genes related to endothelial activation.
Publication Title
Vascular endothelial growth factor activation of endothelial cells is mediated by early growth response-3.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 24 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
The functional balance between brown adipose tissue (BAT) and white adipose tissue (WAT) is important for metabolic homeostasis. We compared the effects of fasting on the gene expression profiles in BAT, WAT and liver, using DNA microarray analysis. Tissues were obtained from rats that had been fed or fasted for 24 h. Taking the false discovery rate (FDR) into account, we extracted the top 1,000 genes that were expressed differentially between fed and fasted rats. In all three tissues, Gene Ontology analysis revealed marked changes in the expression of metabolism category genes and a hypergeometric test demonstrated that within this category, lipid and protein biosynthesis-related genes were down-regulated. These findings indicate simultaneous down-regulation of genes involved in energy-consuming pathways in the BAT, WAT and liver of fasted rats. In the BAT of fasted rats, there was marked up-regulation of genes in the protein ubiquitination category, suggesting that the ubiquitin-proteasome system is involved in saving energy as an adaptation to food shortage.
Publication Title
Up-regulation of genes related to the ubiquitin-proteasome system in the brown adipose tissue of 24-h-fasted rats.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples
GSE109696- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Identification of cancer stem/initiating cells (CSCs/CICs) by a specific marker is useful for diagnosis and therapy of cancer. We have determined that PSF1 which plays a role in DNA replication in lower species is strongly expressed in wide range of normal stem cell population. Here, utilizing the transcriptional activity of PSF1 promoter in tumor cell xenograft model, we show that PSF1high cancer cells display malignant features including high proliferating activity, serial transplantation potential, and metastatic ability those are used for criteria of CSCs/CICs. PSF1high cancer cells localize in perivascular region and genetically display ES cell like signature. Silencing of PSF1 by RNAi inhibited growth of cancer cells mediated by disruption of DNA synthesis and chromosomal segregation. These suggested that PSF1 is a possible maker and a molecular target of CSCs/CICs.
Publication Title
PSF1, a DNA replication factor expressed widely in stem and progenitor cells, drives tumorigenic and metastatic properties.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Endothelial-to-mesenchymal transition (EndMT) in which endothelial cells lose their characteristics and acquire mesenchymal property has recently been recognized as a driver of disease progression in wide range of pathologies. However, the regulatory mechanism of EndMT has not been fully understood. Here, we found that combined knockdown of two ETS family transcription factors, ERG and FLI1, induced EndMT. Hence, we analyzed functions of ERG and FLI1 using gene expression microarray and ChIP-seq to elucidate the regulatory mechanism of EndMT.
Publication Title
Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To identify the possible targets in EMT-acquisition after developing acquired platinum resistance in urothelial carcinoma (UC), we examined the changes in global gene expression before and after development of acquired platinum resistance. Comparing two types of acquired platinum resistant UC cells and their corresponding parent cells, in the end we identified 49 genes (25 up-regulated and 24 down-regulated genes) which were commonly changed in two acquired platinum resistant UC cells.
Publication Title
Acquired platinum resistance involves epithelial to mesenchymal transition through ubiquitin ligase FBXO32 dysregulation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 72 Downloadable Samples
Illumina HiSeq 2500
Description
Circadian clock oscillation emerges in mouse embryo in the later developmental stages. Although circadian clock development is closely correlated with cellular differentiation, the mechanisms of its emergence during mammalian development are not well understood. Here, we demonstrate an essential role of the post-transcriptional regulation of Clock subsequent to the cellular differentiation for the emergence of robust circadian clock oscillation in mouse fetal hearts and mESCs (mouse embryonic stem cells). In mouse fetal hearts, no apparent oscillation of cell-autonomous molecular clock was detectable in around embryonic day (E) 10 whereas robust oscillation was clearly visible in E18 heart. Temporal RNA-seq analysis using mouse fetal hearts reveals much fewer rhythmic genes in E10-12 hearts (63, no clock genes) than E17-19 (483 genes), indicating the lack of functional circadian clocks in E10 mouse fetal hearts. In both mESCs and E10 embryos, CLOCK protein was absent despite the expression of Clock mRNA, which we showed was at least partially due to miRNA-mediated translational suppression of CLOCK. The CLOCK protein is required for the robust molecular oscillation in differentiated cells, and the post-transcriptional regulation of Clock plays a key role in setting the timing for the emergence of the circadian clock oscillation during mammalian development.
Publication Title
Involvement of posttranscriptional regulation of <i>Clock</i> in the emergence of circadian clock oscillation during mouse development.
Sample Metadata Fields
No sample metadata fields
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