MicroRNA expression profiling after short-term exposure to TCDD in zebrafish embryos
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ABSTRACT:
ORGANISM(S): Human alphaherpesvirus 1 Rattus norvegicus Betapolyomavirus hominis Mus musculus Human gammaherpesvirus 8 JC polyomavirus Danio rerio Betapolyomavirus macacae Homo sapiens human gammaherpesvirus 4 Human immunodeficiency virus 1 Human betaherpesvirus 5
PROVIDER: GSE39809 | GEO | 2012/08/02
SECONDARY ACCESSION(S): PRJNA171747
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE38839: MicroRNA expression profiling after short-term exposure to TCDD in zebrafish embryos [agilent and exiqon array data] GSE39808: MicroRNA expression profiling after short-term exposure to TCDD in zebrafish embryos [miRNA-Seq data] Refer to individual Series
2012-08-01 | E-GEOD-39809 | biostudies-arrayexpress
Project description:Although many drugs and environmental chemicals are teratogenic, the mechanisms by which most toxicants disrupt embryonic development are not well understood. microRNAs (miRNAs), single-stranded RNA molecules of ~22 nt that regulate protein expression by inhibiting mRNA translation and promoting mRNA sequestration or degradation, are important regulators of a variety of cellular processes including embryonic development and cellular differentiation. We hypothesized that exposure to xenobiotics can alter miRNA expression and contribute to the mechanisms by which environmental chemicals disrupt embryonic development. To test this hypothesis for one well-known teratogen, we exposed zebrafish embryos to DMSO (0.1%) or TCDD (5 nM) for 1 hr at 30 hours post fertilization (hpf) and measured microRNA expression using several methods at 36 and 60 hpf. TCDD caused strong induction of CYP1A at 36 hpf (62-fold) and 60 hpf (135-fold) as determined by qPCR, verifying the effectiveness of the exposure. microRNA expression profiles were determined using microarrays (Agilent and Exiqon), next-generation sequencing (SOLiD) and real time RT-PCR. The two microarray platforms yielded results that were similar but not identical; both showed significant changes in expression of miR-451, 23a, 23b, 24 and 27e at 60 hpf. Multiple analyses were performed on the SOLiD sequences yielding a total of 16 miRNAs as potentially differentially expressed by TCDD in zebrafish embryos. However, miR-27e was the only miRNA to be identified as differentially expressed by all three methods (both microarrays, SOLiD sequencing, and qPCR). These results suggest that TCDD exposure causes modest changes in expression of microRNAs, including some (miR-451, 23a, 23b, 24 and 27e) that are critical for hematopoiesis and cardiovascular development.
2012-08-02 | GSE39808 | GEO
Project description:MicroRNA expression profiling after short-term exposure to TCDD in zebrafish embryos
| PRJNA171747 | ENA
Project description:Although many drugs and environmental chemicals are teratogenic, the mechanisms by which most toxicants disrupt embryonic development are not well understood. microRNAs (miRNAs), single-stranded RNA molecules of ~22 nt that regulate protein expression by inhibiting mRNA translation and promoting mRNA sequestration or degradation, are important regulators of a variety of cellular processes including embryonic development and cellular differentiation. We hypothesized that exposure to xenobiotics can alter miRNA expression and contribute to the mechanisms by which environmental chemicals disrupt embryonic development. To test this hypothesis for one well-known teratogen, we exposed zebrafish embryos to DMSO (0.1%) or TCDD (5 nM) for 1 hr at 30 hours post fertilization (hpf) and measured microRNA expression using several methods at 36 and 60 hpf. TCDD caused strong induction of CYP1A at 36 hpf (62-fold) and 60 hpf (135-fold) as determined by qPCR, verifying the effectiveness of the exposure. microRNA expression profiles were determined using microarrays (Agilent and Exiqon), next-generation sequencing (SOLiD) and real time RT-PCR. The two microarray platforms yielded results that were similar but not identical; both showed significant changes in expression of miR-451, 23a, 23b, 24 and 27e at 60 hpf. Multiple analyses were performed on the SOLiD sequences yielding a total of 16 miRNAs as potentially differentially expressed by TCDD in zebrafish embryos. However, miR-27e was the only miRNA to be identified as differentially expressed by all three methods (both microarrays, SOLiD sequencing, and qPCR). These results suggest that TCDD exposure causes modest changes in expression of microRNAs, including some (miR-451, 23a, 23b, 24 and 27e) that are critical for hematopoiesis and cardiovascular development.
2012-08-02 | GSE38839 | GEO
Project description:Although many drugs and environmental chemicals are teratogenic, the mechanisms by which most toxicants disrupt embryonic development are not well understood. microRNAs (miRNAs), single-stranded RNA molecules of ~22 nt that regulate protein expression by inhibiting mRNA translation and promoting mRNA sequestration or degradation, are important regulators of a variety of cellular processes including embryonic development and cellular differentiation. We hypothesized that exposure to xenobiotics can alter miRNA expression and contribute to the mechanisms by which environmental chemicals disrupt embryonic development. To test this hypothesis for one well-known teratogen, we exposed zebrafish embryos to DMSO (0.1%) or TCDD (5 nM) for 1 hr at 30 hours post fertilization (hpf) and measured microRNA expression using several methods at 36 and 60 hpf. TCDD caused strong induction of CYP1A at 36 hpf (62-fold) and 60 hpf (135-fold) as determined by qPCR, verifying the effectiveness of the exposure. microRNA expression profiles were determined using microarrays (Agilent and Exiqon), next-generation sequencing (SOLiD) and real time RT-PCR. The two microarray platforms yielded results that were similar but not identical; both showed significant changes in expression of miR-451, 23a, 23b, 24 and 27e at 60 hpf. Multiple analyses were performed on the SOLiD sequences yielding a total of 16 miRNAs as potentially differentially expressed by TCDD in zebrafish embryos. However, miR-27e was the only miRNA to be identified as differentially expressed by all three methods (both microarrays, SOLiD sequencing, and qPCR). These results suggest that TCDD exposure causes modest changes in expression of microRNAs, including some (miR-451, 23a, 23b, 24 and 27e) that are critical for hematopoiesis and cardiovascular development. Small RNA profiles were deteremined in TCDD exposed zebrafish embryos using SOLID sequencing
2012-08-02 | E-GEOD-39808 | biostudies-arrayexpress
Project description:Although many drugs and environmental chemicals are teratogenic, the mechanisms by which most toxicants disrupt embryonic development are not well understood. microRNAs (miRNAs), single-stranded RNA molecules of ~22 nt that regulate protein expression by inhibiting mRNA translation and promoting mRNA sequestration or degradation, are important regulators of a variety of cellular processes including embryonic development and cellular differentiation. We hypothesized that exposure to xenobiotics can alter miRNA expression and contribute to the mechanisms by which environmental chemicals disrupt embryonic development. To test this hypothesis for one well-known teratogen, we exposed zebrafish embryos to DMSO (0.1%) or TCDD (5 nM) for 1 hr at 30 hours post fertilization (hpf) and measured microRNA expression using several methods at 36 and 60 hpf. TCDD caused strong induction of CYP1A at 36 hpf (62-fold) and 60 hpf (135-fold) as determined by qPCR, verifying the effectiveness of the exposure. microRNA expression profiles were determined using microarrays (Agilent and Exiqon), next-generation sequencing (SOLiD) and real time RT-PCR. The two microarray platforms yielded results that were similar but not identical; both showed significant changes in expression of miR-451, 23a, 23b, 24 and 27e at 60 hpf. Multiple analyses were performed on the SOLiD sequences yielding a total of 16 miRNAs as potentially differentially expressed by TCDD in zebrafish embryos. However, miR-27e was the only miRNA to be identified as differentially expressed by all three methods (both microarrays, SOLiD sequencing, and qPCR). These results suggest that TCDD exposure causes modest changes in expression of microRNAs, including some (miR-451, 23a, 23b, 24 and 27e) that are critical for hematopoiesis and cardiovascular development. MicroRNA profiling was performed (N=3 biological replicates per group) using custom designed Agilent miRNA microarrays (8x15K) and exiqon miRCURY LNA microarrays. Custom-made Agilent oligonucleotide miRNA microarrays were designed based on zebrafish mature miRNA sequences from miRbase v.16. Each individual array contained a total of 548 unique probes representing 259 mature miRNAs from zebrafish (245), Fugu rubripes (11) and Tetraodon nigriviridis (3). Exiqon miRNA probes were based on zebrafish miRNA sequences from miRbase v. 12.
2012-08-01 | E-GEOD-38839 | biostudies-arrayexpress
Project description:Although many drugs and environmental chemicals are teratogenic, the mechanisms by which most toxicants disrupt embryonic development are not well understood. MicroRNAs, single-stranded RNA molecules of ~22 nt that regulate protein expression by inhibiting mRNA translation and promoting mRNA sequestration or degradation, are important regulators of a variety of cellular processes including embryonic development and cellular differentiation. Recent studies have demonstrated that exposure to xenobiotics can alter microRNA expression and contribute to the mechanisms by which environmental chemicals disrupt embryonic development. In this study we tested the hypothesis that developmental exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a well-known teratogen, alters microRNA expression during zebrafish development. We exposed zebrafish embryos to DMSO (0.1%) or TCDD (5nM) for 1h at 30hours post fertilization (hpf) and measured microRNA expression using several methods at 36 and 60hpf. TCDD caused strong induction of CYP1A at 36hpf (62-fold) and 60hpf (135-fold) as determined by real-time RT-PCR, verifying the effectiveness of the exposure. MicroRNA expression profiles were determined using microarrays (Agilent and Exiqon), next-generation sequencing (SOLiD), and real-time RT-PCR. The two microarray platforms yielded results that were similar but not identical; both showed significant changes in expression of miR-451, 23a, 23b, 24 and 27e at 60hpf. Multiple analyses were performed on the SOLiD sequences yielding a total of 16 microRNAs as differentially expressed by TCDD in zebrafish embryos. However, miR-27e was the only microRNA to be identified as differentially expressed by all three methods (both microarrays, SOLiD sequencing, and real-time RT-PCR). These results suggest that TCDD exposure causes modest changes in expression of microRNAs, including some (miR-451, 23a, 23b, 24 and 27e) that are critical for hematopoiesis and cardiovascular development.
| S-EPMC3471217 | biostudies-literature
Project description:Benzo(a)pyrene (BaP), a polycyclic aromatic hydrocarbon, is considered a common endocrine disrupting chemical (EDC) with mutagenic and carcinogenic effects. In this work, we evaluated the effects of BaP on the hypothalamo-pituitary-gonadal axis (HPG) of zebrafish embryos. The embryos were treated with 5 and 50 nM BaP from 2.5 to 72 hours post-fertilization (hpf) and obtained data were compared with those from controls. We followed the entire development of gonadotropin releasing hormone (GnRH3) neurons that start to proliferate from the olfactory region at 36 hpf, migrate at 48 hpf and then reach the pre-optic area and the hypothalamus at 72 hpf. Interestingly, we observed a compromised neuronal architecture of the GnRH3 network after the administration of 5 and 50 nM BaP. Given the toxicity of this compound, we evaluated the expression of genes involved in antioxidant activity, oxidative DNA damage and apoptosis and we found an upregulation of these pathways. Consequently, we performed a TUNEL assay and we confirmed an increment of cell death in brain of embryos treated with BaP. In conclusion our data reveal that short-term exposure of zebrafish embryos to BaP affects GnRH3 development likely through a neurotoxic mechanism.
| S-EPMC10138490 | biostudies-literature
Project description:The areca nut-chewing habit is common in Southeast Asia, India, and Taiwan, and arecoline is the most abundant and potent component in the areca nut. The effects of arecoline on birth defects have been explored in many species, including chicken, mice, and zebrafish. The effects of arecoline on embryos after long-term exposure are well established; however, the effects of short-term embryo exposure to arecoline are not understood. Using zebrafish, we study the effects of short-term exposure of arecoline on embryos to model the human habit of areca nut-chewing during early pregnancy. Arecoline, at concentrations from 0.001% to 0.04%, was administered to zebrafish embryos from 4 to 24 hours post fertilization. The morphological changes, survival rates, body length, and skeletal muscle fiber structure were then investigated by immunohistochemistry, confocal microscopy, and conventional electron microscopy. With exposure of embryos to increasing arecoline concentrations, we observed a significant decline in the hatching and survival rates, general growth retardation, lower locomotor activity, and swimming ability impairment. Immunofluorescent staining demonstrated a loose arrangement of myosin heavy chains, and ultrastructural observations revealed altered myofibril arrangement and swelling of the mitochondria. In addition, the results of flow-cytometry and JC-1 staining to assay mitochondria activity, as well as reverse transcription-polymerase chain reaction analyses of functional gene expression, revealed mitochondrial dysfunctions after exposure to arecoline. We confirmed that short-term arecoline exposure resulted in retarded embryonic development and decreased locomotor activity due to defective somitic skeletal muscle development and mitochondrial dysfunction.
| S-EPMC4298148 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-07-02 | GSE244386 | GEO