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Silver nano-colloids disrupt medaka embryogenesis through vital gene expressions

ABSTRACT: Using medaka fish embryo model, toxic effects of silver nanocolloids (SNC, 3.8±1.0nm diameter) on developmental morphology and gene expression profile were investigated. SNC caused morphological changes in embryos including cardiovascular malformations, ischemia, underdeveloped central nervous system and eyes, and kyphosis at exposures of 0.5mg/L and 1.0mg/L.. To determine in vivo distribution of SNC, medaka embryos were exposed to 0.5mg/L for 6 days and subjected to ICP-OES analyses. Silver was detected in medaka embryos and chorion at levels of 16.6±9.3pg and 720±29pg, respectively. TEM analyses showed SNC adhered to the chorion surface and inside the chorion. On investigation of oxidative mechanism, NAC (0.05mM) rescued all embryos by 96-hr post treatment, while 0.5mM GSH did not. NAC blocked lipid peroxidation. Furthermore, medaka oligo DNA microarray and qRT-PCR were used for gene expression profiling in embryos exposed for 48-hr to 0.05mg/L SNC. Six genes relative to embryogenesis and morphogenesis such as ctsL, Tpm1, RBP, mt, atp2a1 and hox6b6 turned out to be affected and their involvement to the above malformations was implied. In conclusion, SNC causes gross malformations in the cardiovascular and central nervous systems in developing medaka embryos through potentially SNC-affected differential expression of a series of genes related to oxidative stress, embryonic cellular proliferation, and morphological development.

ORGANISM(S): Oryzias latipes

PROVIDER: GSE33488 | GEO | 2012/06/17

SECONDARY ACCESSION(S): PRJNA148735

REPOSITORIES: GEO

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Silver nano-colloids disrupt medaka embryogenesis through vital gene expressions

Project description:Using medaka fish embryo model, toxic effects of silver nanocolloids (SNC, 3.8M-BM-11.0nm diameter) on developmental morphology and gene expression profile were investigated. SNC caused morphological changes in embryos including cardiovascular malformations, ischemia, underdeveloped central nervous system and eyes, and kyphosis at exposures of 0.5mg/L and 1.0mg/L.. To determine in vivo distribution of SNC, medaka embryos were exposed to 0.5mg/L for 6 days and subjected to ICP-OES analyses. Silver was detected in medaka embryos and chorion at levels of 16.6M-BM-19.3pg and 720M-BM-129pg, respectively. TEM analyses showed SNC adhered to the chorion surface and inside the chorion. On investigation of oxidative mechanism, NAC (0.05mM) rescued all embryos by 96-hr post treatment, while 0.5mM GSH did not. NAC blocked lipid peroxidation. Furthermore, medaka oligo DNA microarray and qRT-PCR were used for gene expression profiling in embryos exposed for 48-hr to 0.05mg/L SNC. Six genes relative to embryogenesis and morphogenesis such as ctsL, Tpm1, RBP, mt, atp2a1 and hox6b6 turned out to be affected and their involvement to the above malformations was implied. In conclusion, SNC causes gross malformations in the cardiovascular and central nervous systems in developing medaka embryos through potentially SNC-affected differential expression of a series of genes related to oxidative stress, embryonic cellular proliferation, and morphological development. Three of the stage-21 medaka embryos per sample were exposed in triplicate to 0mg/L (control) and 0.05mg/L SNC for 48 hours. Therefore, for each exposure condition nine of the stage-21 embryos were prepared and used in the SNC exposure test.

2012-06-16 | E-GEOD-33488 | biostudies-arrayexpress

Silver nanocolloids affects glycosylation in medaka fish to cause embryonic malformation.

Project description:We observed silver nanocolloids (SNCs) exposure to medaka embryo induced morphological deformities like shortened body and undeveloped head and eyes, and our gene expression analysis using medaka oligo DNA microarray suggested that glycan/glycosylation genes, such as gns and alg2, might be the targets of SNCs' toxicity. Validation studies of gns and alg2 gene expressions by qPCR showed stage-dependent and altered mRNA expression patterns, and their altered expressions were more severe in earlier stages of embryogenesis. A result from structural analysis of glycan revealed that stage 11 was the most sensitive stage to SNCs exposure, and stress seemed to be imposed upon endplasmic reticulum (ER) by SNCs. In fact, qPCR analysis of ER mannosidase demonstrated that N-glycan synthesis in ER was inhibited by SNCs. Overall, this study revealed that SNCs exposure caused embryonic malformations through disruption of glycan biosynthetic pathway in ER.

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Transcriptional responses in newly-hatched Oryzias latipes associated with developmental malformations following diluted bitumen exposure

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Transcriptomic profiles of zebrafish embryos exposed to silver (nanoparticles, bulk and ions) using HT-SuperSAGE in a Illumina GA2 platform

Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms. mRNA profiles of whole zebrafish embryos at 24 and 48 hours post-fertilisation (hpf) exposed to silver in nano, bulk and ionic forms were generated by deep sequencing using HT-SuperSAGE (Illumina GA2).

2013-06-17 | E-GEOD-38125 | biostudies-arrayexpress

Transcriptomic profiles of zebrafish embryos exposed to silver (nanoparticles, bulk and ions) using HT-SuperSAGE in a Illumina GA2 platform

2013-06-17 | GSE38125 | GEO

RNA-seq in Oryzias latipes at stage 24

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RNA-seq in Oryzias latipes at stage 24

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2014-03-25 | E-GEOD-46484 | biostudies-arrayexpress

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Project description:During development, the inherited DNA methylation patterns from the parental gametes needs to be remodeled into a state compatible with embryonic pluripotency. In Zebrafish, this remodeling is achieved by the maternal methylome becoming hypomethylated to match the paternal methylome. However, how this is achieved in medaka (another teleost fish) is currently not known. Moreover, how DNA methylation remodeling is impacted in hybrid organisms, and the effects this may have on their development, is also not known. Here we address these questions by generation whole genome bisulfite sequencing data for zebrafish, medaka and zebrafish medaka embryos.

2023-08-25 | E-MTAB-12535 | biostudies-arrayexpress

Identification of Rx2 binding loci in medaka by iDamID-seq

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2016-10-06 | E-MTAB-4610 | biostudies-arrayexpress

FJ001: Retinoic acid-dependent and -independent gene-regulatory pathways of Pitx3 in meso-diencephalic dopaminergic neurons

Project description:Development of meso-diencephalic dopamine (mdDA) neurons requires the combined actions of the orphan nuclear receptor Nurr1 and the paired-like homeobox transcription factor Pitx3. Whereas all mdDA neurons require Nurr1 for expression of Th and survival, dependence on Pitx3 is only displayed by the mdDA subpopulation that will form the substantia nigra (SNc). Previously, we demonstrated that Pitx3-/- embryos lack the expression of the retinoic acid (RA)-generating enzyme Ahd2, which is normally selectively expressed in the Pitx3-dependent DA neurons of the SNc. Restoring RA-signaling in Pitx3-/- embryos revealed a selective dependence of SNc neurons on the presence of RA for differentiation into Th-positive neurons and maintenance throughout embryonic development. Whereas these data are suggestive of an important developmental role for RA in neurons of the SNc, it remained unclear whether other Nurr1 and Pitx3 target genes depend on RA signaling in a manner similar to Th. In search for genes that were affected in Pitx3-deficient mdDA neurons and restored upon embryonic RA treatment, we provide evidence that Delta-like 1, D2R (Drd2) and TH are regulated by Pitx3 and RA signaling, influencing the mdDA terminal differentiated phenotype. Furthermore, we show that regulation of Ahd2-mediated RA-signaling represents only one aspect of the Pitx3 downstream cascade, since Vmat2, Dat, Ahd2 (Aldh1a1), En1, En2 and Cck were unaffected by RA treatment and are (subset) specifically modulated by Pitx3. In conclusion, our data reveal several RA-dependent and -independent aspects of the Pitx3-regulated gene cascade suggesting that Pitx3 acts on multiple levels in the molecular subset-specification of mdDA neurons. RNA was isolated from dissected ventral midbrains of E14.5 Pitx3-/- and Pitx3+/+ mouse embryos. 3 Experimental samples each consisting of 3 Pitx3-/- ventral midbrains were hybridized to reference RNA derived from 10 Pitx3+/+ ventral midbrains

2011-11-22 | E-GEOD-32940 | biostudies-arrayexpress

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