Transcriptomes performed on left ventricular heart samples from mice of the hybrid mouse diversity panel, a set of over a hundred inbred strains of mice. In this project, the strains were challenged with Isoproterenol, a beta-adrenergic agonist to induce cardiac hypertrophy and failure. Results are useful for the analysis of heart-related traits in mice
Genetic Dissection of Cardiac Remodeling in an Isoproterenol-Induced Heart Failure Mouse Model.
Sex, Specimen part
View SamplesDuring human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4-8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, CTBs isolated from PE and control placentas were cultured for 48 h, enabling differentiation/invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation that resolved in culture. The upregulated genes included SEMA3B. Adding this protein to normal CTBs inhibited invasion and re-created aspects of the phenotype of these cells in PE. Additionally, SEMA3B downregulated VEGF signaling through the PI3K/AKT and GSK3 pathways, effects that were observed in PE CTBs. We propose that, in severe PE, the in vivo environment dysregulates CTB gene expression, the autocrine actions of the upregulated molecules, including SEMA3B, impair differentiation/invasion/signaling and patient-specific factors determine the signs.
Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia.
Specimen part
View SamplesmiRNA-1343 is an uncharacterized miRNA predicted to target a number of genes involved in epithelial cell function including TGF-beta signaling, cell adhesion, and cell proliferation. We transiently overexpressed miRNA-1343 or a non-targeting control miRNA in A549 and 16HBE14o- human airway cell lines. As predicted, RNA-seq following miRNA-1343 overexpression showed significant downregulation of genes involved in these pathways. Furthermore, genes involved in cholesterol and lipid biosynthesis were found to be significantly upregulated by miRNA-1343 overexpression. Overall design: mRNA profiles from A549 and 16HBE14o- cells transiently transfected with miRNA-1343 or a negative control (NC) miRNA, in quintuplicate.
miR-1343 attenuates pathways of fibrosis by targeting the TGF-β receptors.
No sample metadata fields
View SamplesARC (NSC 188491, SMA-491), 4-amino-6-hydrazino-7-beta-d-ribofuranosyl-7H-pyrrolo-(2,3-d)-pyrimidine-5-carboxamide, is a nucleoside analog with profound in vitro anti-cancer activity. First identified in a high-throughput screen for inhibitors of p21 mRNA expression, subsequent experiments showed that ARC also repressed expression of hdm2 and survivin, leading to its classification as a global inhibitor of transcription 1. The following Hu U133 plus 2.0 arrays represent single time point (24 hour) gene expression analysis of transcripts altered by ARC treatment. Arrays for the other compounds (sangivamycin and doxorubicin) are included as comparators.
ARC (NSC 188491) has identical activity to Sangivamycin (NSC 65346) including inhibition of both P-TEFb and PKC.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View SamplesPurpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys. Overall design: mRNA profiles of control and mutant (=Six2-TGC; miR-17~92 flx/flx) embryonic day 16 kidneys were generated by deep sequencing, in triplicate, using Illumina HiSeq2000
MicroRNA-17~92 is required for nephrogenesis and renal function.
No sample metadata fields
View SamplesCLK targets from fly heads using the TIM-GAL4; UAS-CLKGR line
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View Samples6 Timepoint microarray from control strain
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View Samples6 Timepoints from 5073 strain
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View SamplesExperiments performed in S2 cells to identify direct CLK targets
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View Samples