Effect of maternal dioxin exposure on pituitary mRNAs in fetal rats at gestational day 18
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ABSTRACT:
PROVIDER: PRJNA576836 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed pituitary syntheisis of growth hormone during the last fetal stage. We performed a DNA microarray analysis to identify the genes linked to the attenuated expression of GH, using the male and female fetal pituitary at GD18 when the reduced expression of GH started to occur because of TCDD.
2021-01-29 | GSE138694 | 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:Our previous studies have revealed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 μg/kg) at gestational day (GD) 15 reduces the pituitary synthesis of luteinizing hormone (LH) during late fetal and early postnatal period, leading to imprinting of defects in sexual behaviors at adulthood. However, it remains obscure how the attenuation of pituitary LH links to sexual immaturity. To address this issue, we firstly performed a DNA microarray analysis to identify the gene(s) responsible for dioxin-induced sexual immaturity, using the pituitary and hypothalamus of male pups, at the age of postnatal day (PND)70, born from TCDD-treated dams. Among the reduced genes, we focused on gonadotropin-releasing hormone (GnRH) in the hypothalamus, because of its role in sexual behaviors suggested so far. The present study strongly suggests that maternal exposure to TCDD fixes the status of the lowered expression of GnRH in the offspring by reducing steroidogenesis at perinatal stage, and this is the mechanism for the imprinting of defects in sexual behaviors at adulthood.
2013-08-21 | GSE48100 | GEO
Project description:Our previous studies have revealed that treatment of pregnant rats with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 1 M-NM-<g/kg) at gestational day (GD) 15 reduces the pituitary synthesis of luteinizing hormone (LH) during late fetal and early postnatal period, leading to imprinting of defects in sexual behaviors at adulthood. However, it remains obscure how the attenuation of pituitary LH links to sexual immaturity. To address this issue, we firstly performed a DNA microarray analysis to identify the gene(s) responsible for dioxin-induced sexual immaturity, using the pituitary and hypothalamus of male pups, at the age of postnatal day (PND)70, born from TCDD-treated dams. Among the reduced genes, we focused on gonadotropin-releasing hormone (GnRH) in the hypothalamus, because of its role in sexual behaviors suggested so far. The present study strongly suggests that maternal exposure to TCDD fixes the status of the lowered expression of GnRH in the offspring by reducing steroidogenesis at perinatal stage, and this is the mechanism for the imprinting of defects in sexual behaviors at adulthood. Total RNA was isolated from the pituitary and hypothalamus of PND70 male pups born from the dams treated with TCDD (1 M-NM-<g/kg) or vehicle at GD15, using an RNeasy Mini Kit (QIAGEN). To identify the gene(s) the altered expression of which is fixed and linked to defects in sexual behaviors, the profile of gene expression was analyzed using the Illumina RatRef-12 Expression BeadChip. This series includes two dataset; hypothalamic and pituitary samples (each case; N=3x2). The normalization applied each dataset.
2013-08-21 | E-GEOD-48100 | biostudies-arrayexpress
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: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:Effect of dioxin on pituitary mRNAs in maternal rats at postpartum day 7
| PRJNA560677 | ENA
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:To identify the gene expression change during pituitary aging, we did the RNA-seq of pituitary from 2-3 months young mice and 18-24 months old mice. The mRNA level of different genes were analyzed.
2022-10-14 | GSE215110 | GEO
Project description:There is a growing body of evidence that inadequate maternal nutrition during gestation can have immediate and life-long effects on offspring. However, little is known about the reproductive effects of maternal gestational nutrition in offspring males. Here, using a sheep model of poor maternal nutrition (restricted- or over-feeding) during gestation, we found that poor maternal gestational nutrition does not affect semen characteristics (i.e. volume, sperm concentration, pH, sperm motility, sperm morphology) and scrotal circumference in offspring. However, by evaluating associations between poor maternal gestational nutrition and altered small non-cording RNAs (sncRNAs) and DNA methylation in offspring sperm, we demonstrated that poor maternal gestational nutrition alters sperm sncRNA composition and expression. Whole genome bisulfite sequencing further identified genomic regions with increased or decreased DNA methylation in sperm in response to poor maternal gestational nutrition. These findings imply that maternal diet-induced epigenetic errors can accumulate in sperm to worsen developmental outcomes of future generations.
2024-04-04 | GSE225985 | GEO