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Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment

ABSTRACT: Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment

PROVIDER: PRJNA319581 | ENA |

REPOSITORIES: ENA

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Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [imidacloprid]

Project description:Neonicotinoids are considered safe because of their low affinities to mammalian nicotinic acetylcholine receptors (nAChRs) relative to insect nAChRs. However, because of importance of nAChRs in mammalian brain development, there remains a need to establish the safety of chronic neonicotinoid exposures with regards to children’s health. Here we examined the effects of long-term (14 days) and low dose (1 μM) exposure of neuron-enriched cultures from neonatal rat cerebellum to nicotine and two neonicotinoids: acetamiprid and imidacloprid. Immunocytochemistry revealed no differences in the number or morphology of immature neurons or glial cells in any group versus untreated control cultures. However, a slight disturbance in Purkinje cell dendritic arborization was observed in the exposed cultures. Next we performed transcriptome analysis on total RNAs using microarrays, and identified significant differential expression (p < 0.05, q < 0.05, ≥1.5 fold) between control cultures versus nicotine-, acetamiprid-, or imidacloprid-exposed cultures in 34, 48, and 67 genes, respectively. Common to all exposed groups were nine genes essential for neurodevelopment, suggesting that chronic neonicotinoid exposure alters the transcriptome of the developing mammalian brain in a similar way to nicotine exposure. Our results highlight the need for further careful investigations into the effects of neonicotinoids in the developing mammalian brain.

2016-10-04 | GSE80653 | GEO

Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [nicotine]

2016-10-04 | GSE80638 | GEO

Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [acetamiprid]

2016-10-04 | GSE80652 | GEO

Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-10-04 | GSE80656 | GEO

Rattus norvegicus

Project description:Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [acetamiprid]

| PRJNA319579 | ENA

Rattus norvegicus

Project description:Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [imidacloprid]

| PRJNA319580 | ENA

Rattus norvegicus

Project description:Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment [nicotine]

| PRJNA319577 | ENA

GNPS Integrated non-targeted lipidomics and metabolomics analyses for fluctuations of neonicotinoids imidacloprid and acetamiprid on Neuro-2a cells

Project description:These data and results are supplementary material for the manuscript: Integrated non-targeted lipidomics and metabolomics analyses for fluctuations of neonicotinoids imidacloprid and acetamiprid on Neuro-2a cells

2021-05-01 | MSV000087346 | GNPS

Transcriptional profiling of a novel mutant resistant to imidacloprid and DDT

Project description:Deep-sequencing analysis of mRNA expression differences between imidacloprid and DDT resistant mutant line and iso31 (w1118) susceptible line have been obtained. A total of 357 transcripts were found to be differently expressed, with 150 upregulated and 207 downregulated genes in the resistant line.

2012-06-28 | GSE28560 | GEO

Perinatal exposure to nicotine alters spermatozoal DNA methylation near genes controlling nicotine action

Project description:Perinatal smoke/nicotine exposure alters lung development and causes asthma in exposed offspring, transmitted transgenerationally. The mechanism underlying the transgenerational inheritance of perinatal smoke/nicotine-induced asthma remains unknown, but germline epigenetic modulations may play a role. Using a well-established rat model of perinatal nicotine-induced asthma, we determined the DNA methylation pattern of spermatozoa of F1 rats exposed perinatally to nicotine in F0 gestation. To identify differentially methylated regions (DMRs), reduced representation bisulfite sequencing was performed on spermatozoa of F1 litters. The top regulated gene body and promoter DMRs were tested for lung gene expression levels, and key proteins involved in lung development and repair were determined. The overall CpG methylation in F1 sperms across gene bodies, promoters, 5’UTRs, exons, introns, and 3’UTRs was not affected by nicotine exposure. However, the methylation levels were different between the different genomic regions. 81 CpG sites, 16 gene bodies, and 3 promoter regions were differentially methylated. Gene enrichment analysis of DMRs revealed pathways involved in oxidative stress, nicotine response, alveolar and brain development, and cellular signaling. Among the DMRs, Dio1 and Nmu were the most hypermethylated and hypomethylated genes, respectively. Gene expression analysis showed that the mRNA expression and DNA methylation were incongruous. Key proteins involved in lung development and repair were significantly different (FDR < 0.05) between the nicotine and placebo-treated groups. Our data show that DNA methylation is remodeled in offspring spermatozoa upon perinatal nicotine exposure. These epigenetic alterations may play a role in transgenerational inheritance of perinatal smoke/nicotine induced asthma.

2021-05-17 | GSE173898 | GEO

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