Analysis of murine cardiomyocyte cell line HL-1 treated with Ivermectin or Importazole. Results provide insight into the pathways regulated by the treatments. Overall design: RNA-seq of mouse HL-1 cardiomyocytes treated with vehicle (DMSO), Ivermectin, or Importazole for 24 hours, in triplicate, using Ion Proton System.
Antihypertrophic Effects of Small Molecules that Maintain Mitochondrial ATP Levels Under Hypoxia.
Specimen part, Cell line, Treatment, Subject
View SamplesMedulloblastoma (MB) is the most common malignant brain tumor in children, among whom overexpression or amplification of MYC oncogenes has been associated with poor clinical outcome. Although the MYC functions during normal development and oncogenesis in various systems have been extensively investigated, the transcriptional targets mediating MYC effects in MB are still elusive. Their identification and roles during MB onset and progression are important and will ultimately suggest novel potential therapeutic targets. cDNA microarray analysis was used to compare the effects of overexpressing and silencing MYC on the transcriptome of a MB-derived cell line. We identified 209 genes with potential relevance to MYC-dependent cellular responses in MB. Among the MYC-responsive genes, we found members of the bone morphogenetic protein (BMP) signaling pathway, which plays a crucial role during the development of the cerebellum. In particular, the cytokine gene BMP7 was identified as a direct target of MYC in MB cells. Similar to the effect induced by BMP7 silencing by siRNA, the use of a small-molecule inhibitor of the BMP/SMAD signaling pathway reduced cell viability in a panel of MB cells. Altogether, our findings indicate that high MYC levels drive BMP7 expression in MB to induce pro-survival and pro-proliferative cellular pathways. This observation suggests that targeting the BMP/SMAD pathway may be a new therapeutic concept for the treatment of childhood MB.
Bone morphogenetic protein-7 is a MYC target with prosurvival functions in childhood medulloblastoma.
Specimen part, Cell line
View SamplesAnalysis of expression changes in renal collecting duct epithelial cells by adenoviral mediated Krppel like transcription factor 5 (KLF5) overexpression. KLF5 is a key regulator of static and inflammatory stage in renal collecting duct epithelial cells. We thought these results provide insights into downstream genes of KLF5 in renal collecting duct epithelial cells.
Renal collecting duct epithelial cells regulate inflammation in tubulointerstitial damage in mice.
Specimen part, Cell line
View SamplesGlioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation.
Glioma initiating cells form a differentiation niche via the induction of extracellular matrices and integrin αV.
No sample metadata fields
View SamplesTo elucidate the effects of altered dietary carbohydrate and fat balance on liver and adipose tissue transcriptomes,
Transcriptomic responses of the liver and adipose tissues to altered carbohydrate-fat ratio in diet: an isoenergetic study in young rats.
No sample metadata fields
View SamplesMastication enhances brain function and even mental health, but little is known molecular basis underlying the effects of chewing on neural development in early childhood we conducted experiment with rats fed a with soft or hard chow diet immediately after weaning and investigated the expression of genes were investigated after another 8 days of breeding.
Short-term mastication after weaning upregulates GABAergic signalling and reduces dendritic spine in thalamus.
Sex, Age
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.
Specimen part
View SamplesPurpose: RNA-Seq analysis can help identify large set of differentially expressed genes at a time. We performed RNA-Seq analysis to identify differentially expressed genes in the PBMCs of war veterans suffering from PTSD. Methods: Total RNA from PBMCs from PTSD +ve and -ve individuals were used for RNA-Seq analysis. Results: We obtained, on average, ~60 millions reads per sample. More than 70% of the reads were mapped to human genome. Functional analysis of the differentially expressed genes (362) revealed dysregulation in immune system network. Conclusions: Our present study provides further proof that immune system related genes and pathways are dysregulated in PTSD PBMCs. Overall design: RNA-Seq was performed with RNA from 5 each control and PTSD individuals. PBMCs collected within one hour of blood draw were used for RNA isolation. 1 ug of total RNA was used for library synthesis and sequenced in a HighSeq 2000 illumina instrument at Tufts University.
Decreased AGO2 and DCR1 in PBMCs from War Veterans with PTSD leads to diminished miRNA resulting in elevated inflammation.
Specimen part, Subject
View SamplesEndothelial-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.
Downregulation of ERG and FLI1 expression in endothelial cells triggers endothelial-to-mesenchymal transition.
No sample metadata fields
View SamplesIn order to find the difference between human lung tissue-derived fibroblasts and human vascular adventitial fibroblasts for enhancing tumor formation ablity of human lung adenocarcinoma cell line A549, we found that human vascular adventitial fibroblasts enhance A549 tumor formation in vivo compared to human lung tissue-derived fibroblasts. To find the responsible genes for this phenomena, we used microarray analysis to find the expression difference between lung tissue-derived fibroblasts and vascular adventitial fibroblas
Podoplanin-positive fibroblasts enhance lung adenocarcinoma tumor formation: podoplanin in fibroblast functions for tumor progression.
Specimen part
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