Effect of dioxin on hypothalamic mRNAs in maternal rats at postpartum day 7
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PROVIDER: PRJNA560676 | ENA |
REPOSITORIES: ENA
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Project description:Effect of dioxin on pituitary mRNAs in maternal rats at postpartum day 7
| PRJNA560677 | ENA
Project description:Effect of dioxin on maternal rats at postpartum day 7
| PRJNA560678 | ENA
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the hypothalamus, which regulates the pituitary prolactin synthesis, of lactating dam rats.
2020-06-19 | GSE135931 | GEO
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the pituitary of lactating dam rats.
2020-06-19 | GSE135932 | GEO
Project description:Effect of maternal dioxin exposure on pituitary mRNAs in fetal rats at gestational day 18
| PRJNA576836 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-06-20 | GSE135933 | GEO
Project description: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.
2011-10-01 | GSE32459 | GEO
Project description: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. Pregnant Wistar rats were orally treated with TCDD (1 µg/kg in corn oil) at gestational day (GD)15. Then, the total RNA was extracted from the fetal pituitary and hypothalamus at GD20. To identify the target genes the alteration of which contributes to a reduction in fetal gonadotropin β-subunit, the profile of gene expression was analyzed using the Illumina RatRef-12 Expression BeadChip.
2011-09-30 | E-GEOD-32459 | biostudies-arrayexpress
Project description:The dioxin congener 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide range of toxic effects in rodent species, all of which are mediated by a ligand-dependent transcription-factor, the aryl hydrocarbon receptor (AHR). The Han/Wistar (Kuopio) (H/W) strain shows exceptional resistance to many TCDD-induced toxicities; the LD50 of >9600 µg/kg for H/W rats is higher than for any other wild-type mammal known. We have previously shown that this resistance primarily results from H/W rats expressing a variant AHR isoform that has a substantial portion of the AHR transactivation domain deleted. Despite this large deletion, H/W rats are not entirely refractory to the effects of TCDD; the variant AHR in these animals remains fully competent to up-regulate well-known dioxin-inducible genes. TCDD-sensitive (Long-Evans, L-E) and resistant (H/W) rats were treated with either corn-oil (with or without feed-restriction) or 100 µg/kg TCDD for either four or ten days. Hepatic transcriptional profiling was done using microarrays, and was validated by RT-PCR analysis of 41 genes. . A core set of genes was altered in both strains at all time points tested, including CYP1A1, CYP1A2, CYP1B1, Nqo1, Aldh3a1, Tiparp, Exoc3, and Inmt. Outside this core, the strains differed significantly in the breadth of response: three-fold more genes were altered in L-E than H/W rats. At ten days almost all expressed genes were dysregulated in L-E rats, likely reflecting emerging toxic responses. Far fewer genes were affected by feed-restriction, suggesting that only a minority of the TCDD-induced changes are secondary to the wasting syndrome.
2011-11-14 | GSE13513 | GEO
Project description:Female lactating mammals undergo many physiological and behavioral changes postpartum to care for newborn offspring and meet the increased caloric demands of milk production. To uncover the neural correlates of these postpartum adaptations, we investigated how gene expression in two hypothalamic regions -- the arcuate nucleus (ARC) and the medial preoptic area (MPOA) -- is regulated by food deprivation and lactation. To this end, we employed 10x Genomics scRNA-seq in the ARC and MPOA of 4 groups of age-matched female mice: sated virgins (VS), fasted virgins (VF), sated mothers (MS), and fasted mothers (MF).
2025-05-05 | GSE295610 | GEO