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SOFT file
| Title / Description |
Dioxin effect on the pituitary and hypothalamic expression of genes in male fetal Wistar rats |
| Accession |
GSE32459
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| Summary |
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes the many forms of reproductive toxicity, such as defects in sexual behaviors, in pups of which mother is exposed to this substance at lower doses. However, the mechanism underlying these defects remains to be clarified in spite of many researches conducted so far. Our previous studies have revealed that maternal treatment with TCDD attenuates the production of pituitary gonadotropins [luteinizing hormone (LH) and follicle-stimulating hormone] in the late fetuses, leading to the impairment of sexual behavior in adulthood. To identify the target genes for a fetal reduction in gonadotropin β-subunit, we performed DNA microarray analysis using the fetal pituitary and its regulatory organ, the hypothalamus. The result showed that TCDD induced histone deacetylases (HDACs), and altered the expression of genes including gonadotropin-releasing hormone and activin signaling in the fetal pituitary. Moreover, our data indicated that the increased deacetylation of histone due to HDAC induction plays a critical role for a dioxin-induced attenuation of LHβ in the fetal pituitary. This study suggests a novel molecular mechanism explaining dioxin-produced reproductive toxicity. |
| Organism |
Rattus norvegicus |
| Platform |
GPL6101 |
| Normalized |
False |
| Parsed SOFT file |
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Metadata
| Differential expression method |
Characteristic Direction
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| Cutoff |
500 |
| Cell_type |
Hypothalamus |
| Drug_id |
CID 15625 |
| Drug_name |
Dioxin |
| Organism |
Rat |
Visualizations
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| Hierarchical clustering |
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External Links and Downloads
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Gene lists
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Enrichr
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L1000CDS2
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PAEA
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Crowdsourcing |
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