Neonatal hearts (P2) from wildtype, miR-1-1 null and miR-1-2 +/-: miR-1-1 +/- double heterozygote animals were isolated and total RNA was extracted with TRIzol (Invitrogen), following the manufacturers suggested protocol.
microRNA-1 regulates sarcomere formation and suppresses smooth muscle gene expression in the mammalian heart.
Specimen part
View SamplesWe used microarrays to study the effect of Chd1 loss of function in mouse ES cells.
Chd1 regulates open chromatin and pluripotency of embryonic stem cells.
Cell line
View SamplesEnteric glial cells (EGCs) are the main constituent of the enteric nervous system and share similarities with astrocytes from the central nervous system including their reactivity to an inflammator microenvironment. In this study we isolated GFAP-positive myenteric glia from FVB/hGFAP-eGFP transgenic postnatal day 7 mice. Following cell sorting for the eGFP reporter, GFAP-positive EGCs were cultured for 3 weeks to generate neurosphere-like bodies. This cell culture was stimulated with LPS for 48 h and cells were employed for gene expression profiling. LPS-stimulated cell cultures were compared to untreated control cell cultures. Enriched GFAP+ EGC cultures secreted increased levels of prominent inflammatory cytokines upon LPS stimulation. Further, in vitro cultures were compared to GFAP-eGFP-positive cells directly analyzed after cell sorting of small intestinal LMMP digests (in vivo) to assess alterations in transcriptomic profiles due to the in vitro culture.
Activation of Myenteric Glia during Acute Inflammation In Vitro and In Vivo.
Specimen part
View SamplesExposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation.
Aryl hydrocarbon receptor-mediated down-regulation of sox9b causes jaw malformation in zebrafish embryos.
No sample metadata fields
View SamplesMicroarrays were conducted to asses the effect of Stb3 deletion in immediate transcriptional induction in response to glucose
Stb3 binds to ribosomal RNA processing element motifs that control transcriptional responses to growth in Saccharomyces cerevisiae.
No sample metadata fields
View SamplesRetinoic acid (RA) and 2,3,7,8-tetrachlorodibenzo-p-dioxin activate distinct ligand-dependent transcription factors, and both cause cardiac malformation and heart failure in zebrafish embryos. We hypothesized that they cause this response by hyperactivating a common set of genes critical for heart development. To test this, we used microarrays to measure transcripts changes in hearts isolated from zebrafish embryos 1,2,4 and 12 h after exposure to 1M RA. We used hierarchical clustering to compare the transcriptional responses produced in the embryonic heart by RA and TCDD. We could identify no early responses in common between the two agents. However, at 12 h both treatments produced a dramatic downregulation of a common cluster of cell cycle progression genes, which we term the Cell Cycle Gene Cluster (CCGC). This was associated with a halt in heart growth. These results suggest that RA and TCDD ultimately trigger a common transcriptional response associated with heart failure, but not through the direct activation of a common set of genes. Among the genes rapidly induced by RA was Nr2F5, a member of the COUP-TF family of transcription repressors. We found that induction of Nr2F5 was both necessary and sufficient for the cardiotoxic response to RA.
Comparative genomics identifies genes mediating cardiotoxicity in the embryonic zebrafish heart.
No sample metadata fields
View SamplesThe purpose of this experiment is to understand which transcripts are differentially expressed following exposure to TCDD.
TCDD inhibits heart regeneration in adult zebrafish.
Treatment
View SamplesFor analysis of gene expression changes in the zebrafish larvae heart in response to TCDD exposure, three replicate samples of heart tissue were collected at 73, 74, 76 and 84 hours post fertilization from larvae exposed to 1 ng/ml TCDD or vehicle from 72 - 73 hours post fertilization. For analysis of gene expression changes in the extracardiac tissue in response to TCDD exposure, three replicate samples of zebrafish larvae bodies with the heart tissue removed were collected at 73, 74, 76 and 84 hours post fertilization from larvae exposed to 1 ng/ml TCDD or vehicle from 72 - 73 hours post fertilization.
Aryl hydrocarbon receptor activation produces heart-specific transcriptional and toxic responses in developing zebrafish.
Age, Specimen part, Compound, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Lhx5 controls mamillary differentiation in the developing hypothalamus of the mouse.
Specimen part, Treatment
View SamplesLhx5 mutant mouse embryos show loss of a neuronal nucleus of the brain called the mamillary body and essential for the formation of memories. We wanted to identify the genes that are responsible for the normal development of the mammillary body.
Lhx5 controls mamillary differentiation in the developing hypothalamus of the mouse.
Specimen part
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