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ABSTRACT: Effects of 2,3',4,4'5-Pentachlorobiphenyl Exposure during Pregnancy on Maturation of Offspring Oocytes in Mice

PROVIDER: PRJNA551196 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9596963_1.fastq.gz	Fastqsanger.gz
	SRR9596963_2.fastq.gz	Fastqsanger.gz
	SRR9596964_1.fastq.gz	Fastqsanger.gz
	SRR9596964_2.fastq.gz	Fastqsanger.gz
	SRR9596965_1.fastq.gz	Fastqsanger.gz

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Effects of 2,3',4,4'5-Pentachlorobiphenyl Exposure during Pregnancy on Maturation of Offspring Oocytes in Mice

Project description:Effects of 2,3',4,4'5-Pentachlorobiphenyl Exposure during Pregnancy on Maturation of Offspring Oocytes in Mice

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Effects of 2,3',4,4'5-Pentachlorobiphenyl Exposure during Pregnancy on Maturation of Offspring Oocytes in Mice

Project description:To investigate the effect of prenatal exposure of PCB118 on the maturation process of offspring mouse oocytes, we performed genome-wide transcriptome sequencing of mouse oocytes from each group,providing evidence for the effect of PCB118 exposure during pregnancy on the quality of offspring oocyte.

2019-10-29 | GSE133488 | GEO

Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

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Impact of mothers' early life exposure to low or high folate on progeny outcome and DNA methylation patterns

Project description:The dynamic patterning of DNA and histone methylation during oocyte development presents a potentially susceptible time for epigenetic disruption due to early life environmental exposure of future mothers. We investigated whether maternal exposure to folic acid deficient (FD) and supplemented (FS) diets starting in utero could affect oocytes and cause adverse developmental and epigenetic effects in next generation progeny. Female BALB/c mice (F0) were placed on one of four amino acid defined diets for 4 weeks before pregnancy and throughout pregnancy and lactation: folic acid control (rodent daily recommended intake or DRI; Ctrl), 7−fold folic acid deficient (7FD), 10−fold folic acid supplemented (10FS) or 20−fold folic acid supplemented (20FS) diets. F1 female pups were weaned onto Ctrl diets, mated to produce the F2 generation, and the F2 offspring were examined at E18.5 for developmental and epigenetic abnormalities. Resorption was increased and litter sizes decreased amongst F2 E18.5 day litters in the 20FS group. Increases in abnormal embryo outcomes were observed in all three FD and FS groups. Subtle genome-wide DNA methylation alterations were found in the placentas and brains of F2 offspring in the 7D, 10FS and 20FS groups; in contrast, global and imprinted gene methylation were not affected. The findings show that early life female environmental exposures to both low and high folate prior to oocyte maturation can compromise oocyte quality, adversely affecting offspring of the next generation, in part by altering DNA methylation patterns.

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Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.

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Expression data from adult mouse testis exposed to cigarette smoke in utero

Project description:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility. C57BL/6 5 week-old female mice were exposed via the nose-only to cigarette smoke [twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, five times per week, for 12-18 weeks]. Each exposure lasted 60 minutes. Control mice received room air. In total, 27 mice underwent cigarette smoke exposure. Eleven week-old female mice exposed to cigarette smoke for 6 weeks were separated into groups of three and housed with a single control stud male aged 7-8 weeks with proven fertility for a maximum of 12 weeks. Females were monitored every second day for post-coital plugs and pregnancy. Pregnant females were separated into single cages and litter sizes/pup weights recorded. Smoke exposure via dams continued throughout mating/pregnancy/lactation until weaning of pups at 21days post birth. The testis of exposed offspring were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip

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Expression data from mouse lungs exposed in-utero and/or as an adult to second-hand smoke (SHS)

Project description:Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs. Left lungs from Balb/c male mice were collected at 15 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on their smoke exposure status, there are 4 groups of mice, each exposed in-utero to filtered-air or SHS and as an adult to filtered-air or SHS. We extracted RNA from 4 animals from each group for microarray analysis (N = 16 samples).

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Project description:In order to establish an obese mouse model, female mice were continuously fed with a high-fat diet (HFD) or a normal diet (control) for 16 weeks beginning at three weeks of age. In this paper, these mice are termed ‘HFD mice’ and ‘control mice’, respectively. Accordingly, we call their oocytes ‘HFD oocytes’ and ‘control oocytes’. Substantial evidence indicates that the effects of maternal obesity on embryo/offspring development can be attributed to factors within the oocyte (9). To identify such potential effectors, we performed a comparative proteomic analysis of ovulated MII oocytes from control and HFD mice.

2018-05-24 | PXD006641 | Pride

Gene expression in the F1 and F2 mouse hippocampus with intrauterine hyperglycemia exposure

Project description:Studies on human and animals suggest associations between gestational diabetes mellitus (GDM) with impaired cognitive performance in offspring. Using a mouse model of diabetes during pregnancy, we found that intrauterine hyperglycemia exposure resulted in memory impairment in both the first filial (F1) males and the second filial (F2) males from the F1 male offspring. The effects of intrauterine hyperglycemia exposure on F1 and F2 hippocampus gene expression were also examined.

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Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.

Project description:SHS exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero SHS exposure and adult (19-23 weeks) OVA challenge in 23-week mouse lungs. Left lungs from Balb/c male and female mice were collected at 23 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on the gender differences and in-utero exposure status, there are 4 groups of mice, females and males, exposed in-utero to filtered-air or SHS. All were exposure to OVA (19-23 weeks). We extracted RNA from 4 animals from each group for microarray analysis (total N = 16 samples).

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