Mus musculus
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ABSTRACT:
PROVIDER: PRJNA296364 | ENA |
REPOSITORIES: ENA
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Project description:A non-optimal fetal environment is known to cause low birth weight, which has been epidemiologically associated with a greater risk of adult diseases. Maternal undernutrition in animal models has also revealed the increased risks for adult diseases in the offspring. In this study, pregnant mice underwent overnight food deprivation at gestation day (GD)17 or 50% food restriction (FR) from GD10 to GD17, and the fetal brains were examined for global changes in gene expression by DNA microarray analysis utilizing the dye-swap approach. We present here a list of candidate genes from the fetal brain that might be responsible for developmental origins of health and disease. For food deprivation (FD), the pregnant mice were deprived of the food for overnight before lights were turned off on GD17. For food restriction (FR), pregnant mice were exposed to 50% food restriction (FR) from GD 10 to 17 and caesarean section was performed between 10:00-12:00 AM on GD18. Amount of CE-2 chow supplied to FR group was calculated as 50% of CE-2 consumed by control group each gestation day. Control group was supplied with chow ad libitum. Pregnant mice were sacrificed by cervical dislocation, and the fetuses were taken out and anesthetized on ice cold phosphate-buffered saline. The fetuses were dissected under a dissection microscope, and fetal tissues are carefully removed avoiding any other tissues contamination. The brain was collected from control (n=5) and FD (n=5) or FR (n=5) fetuses, and immediately frozen by immersion in liquid nitrogen. For DNA microarray analyses, the total RNA was extracted, quality and quantity determined, and total RNA from each sample (control and treatment) in each group was pooled, followed by established protocols for genome wide expression changes for both FD and FR samples using a 60-mer probes (4 x 44K (41,090 gene probes), mouse whole genome, Agilent) DNA chip by the dye-swap approach.
2015-09-19 | E-GEOD-73202 | biostudies-arrayexpress
Project description:A non-optimal fetal environment is known to cause low birth weight, which has been epidemiologically associated with a greater risk of adult diseases. Maternal undernutrition in animal models has also revealed the increased risks for adult diseases in the offspring. In this study, pregnant mice underwent overnight food deprivation at gestation day (GD)17 or 50% food restriction (FR) from GD10 to GD17, and the fetal brains were examined for global changes in gene expression by DNA microarray analysis utilizing the dye-swap approach. We present here a list of candidate genes from the fetal brain that might be responsible for developmental origins of health and disease.
2015-09-19 | GSE73202 | GEO
Project description:Non-optimal fetal environments resulting in low birth weight have epidemiologically been associated with a higher risk of adult diseases. In animal models, maternal undernutrition has successfully demonstrated that offspring owed increased risks for adult diseases. In mice, shorten life span was also demonstrated in offspring following maternal undernutrition. In the present study, we treated pregnant mice with 50% food restriction (FR), and performed global gene expression and promotor DNA methylation profiling on the fetal livers. Considering that effects of food restriction is opposite between before and after birth, we further searched genes which are regulated oppositely against adult calorie restriction (CR) and commonly against aging. Among searched genes, trib1 has already been demonstrated to contribute to a risk of cardiovascular disease, hypertriglyceridaemia and insulin resistance. The present result suggests that expression of trib1 is affected by maternal nutrition, and is one of the most responsible genes for developmental origins of metabolic syndrome. In addition, lepr was also down-regulated by maternal FR, suggested a potential role of this gene in induction of obesity and diabetes. Promotor DNA methylation profiling as well as gene expression profiling revealed that glucocorticoid receptor target genes were regulated by maternal FR. This finding supports previous studies that suggest an important role for glucocorticoid in developmental origins of metabolic syndrome. In the immune system, most of the genes related to interferon were down-regulated in their expression with up-regulation of their promoter DNA methylation. The profiling also suggested diminished NF-κB signalling. These results suggested that maternal FR affected development of the immune system. We presented here a list of genes responsible for developmental origins of health and disease, which were regulated oppositely against adult CR, and commonly against aging, and also affected their promotor DNA methylation. The present list hopefully contributes to prediction of risks for non communicable diseases, and also prediction of prenatal environment of nutrition from offspring materials. Here we carried out global gene expression profiling analysis on the fetal mouse liver following maternal 50% FR. Considering that opposite effects of nutrition between the fetus and adult, we further analyzed our fetal array data by comparing with data from their mothers, and array data on the effect of CR and aging in previous reports using adult rodent tissues. In addition, we performed global DNA methylation analysis using mouse promoter microarray, and compared the results with data of the gene expression analysis. Finally, we presented a list of candidate genes responsible for DOHaD.
2013-11-19 | E-GEOD-52517 | biostudies-arrayexpress
Project description:Non-optimal fetal environments resulting in low birth weight have epidemiologically been associated with a higher risk of adult diseases. In animal models, maternal undernutrition has successfully demonstrated that offspring owed increased risks for adult diseases. In mice, shorten life span was also demonstrated in offspring following maternal undernutrition. In the present study, we treated pregnant mice with 50% food restriction (FR), and performed global gene expression and promotor DNA methylation profiling on the fetal livers. Considering that effects of food restriction is opposite between before and after birth, we further searched genes which are regulated oppositely against adult calorie restriction (CR) and commonly against aging. Among searched genes, trib1 has already been demonstrated to contribute to a risk of cardiovascular disease, hypertriglyceridaemia and insulin resistance. The present result suggests that expression of trib1 is affected by maternal nutrition, and is one of the most responsible genes for developmental origins of metabolic syndrome. In addition, lepr was also down-regulated by maternal FR, suggested a potential role of this gene in induction of obesity and diabetes. Promotor DNA methylation profiling as well as gene expression profiling revealed that glucocorticoid receptor target genes were regulated by maternal FR. This finding supports previous studies that suggest an important role for glucocorticoid in developmental origins of metabolic syndrome. In the immune system, most of the genes related to interferon were down-regulated in their expression with up-regulation of their promoter DNA methylation. The profiling also suggested diminished NF-κB signalling. These results suggested that maternal FR affected development of the immune system. We presented here a list of genes responsible for developmental origins of health and disease, which were regulated oppositely against adult CR, and commonly against aging, and also affected their promotor DNA methylation. The present list hopefully contributes to prediction of risks for non communicable diseases, and also prediction of prenatal environment of nutrition from offspring materials.
2013-11-19 | GSE52517 | GEO
Project description:Seeking genes responsible for developmental origins of health and disease from the fetal mouse liver following maternal food restriction
| PRJNA229158 | ENA
Project description:Human epidemiological evidence has led scientists to theorize that undernutrition during gestation is an important early origin of adult diseases. Animal models have successfully demonstrated that maternal diet could contribute to some of adult diseases. Undernutrition is perceived harmful in pregnant women whereas calorie restriction is a strategy proven to extend healthy and maximum life span in adult. This diagrammatically opposite effect of nutritional condition might provide us hints to search for genes underlying health conditions. Here, we have initiated a study examining the effect of undernutrition on maternal and fetal livers, utilizing high-throughput DNA microarray analysis for screening genome-wide changes in their transcriptomes. Briefly, pregnant mice were exposed to food deprivation (FD) on gestation day (GD) 17, and caesarean section was performed on GD18. Control mice were supplied with chow ad libitum till sacrifice. Total RNA extracted from mother and fetal livers for each control and treatment (FD) was analyzed with an Agilent mouse whole genome DNA chip. Total of 3058 and 3126 up (>1.5 fold)- and down (<0.75 fold)-regulated genes, and 1475 and 1225 up- (>1.5 fold)- and down (<0.75 fold)-regulated genes showed differential expression at the mRNA level, in the maternal and fetal livers, respectively. Interestingly, 103 genes up-regulated in mother were down-regulated in fetus, whereas 108 down-regulated maternal genes were up-regulated in fetus; these 211 genes are potential candidates related to longevity or health. The role of some of these genes, in context of the proposed mechanisms for developmental origins of health and disease is discussed. Comparison between mouse control and FD livers in fetus and mother was performed. Five to ten biological replicates were used, and pooled total RNA from each condition (control and FD) was dye-swaped.
2011-04-01 | E-GEOD-28175 | biostudies-arrayexpress
Project description:Seeking genes responsible for developmental origins of health and disease from the fetal mouse liver following maternal food restriction [Methylation]
| PRJNA229161 | ENA
Project description:Seeking genes responsible for developmental origins of health and disease from the fetal mouse liver following maternal food restriction [Expression]
| PRJNA215709 | ENA
Project description:Non-optimal fetal environments resulting in low birth weight have epidemiologically been associated with adult diseases. In animal models, maternal undernutrition has successfully demonstrated increased risks for adult diseases. In the present study, we treated pregnant mice with 50% food restriction (FR), and performed global gene expression and promotor DNA methylation profiling on the fetal livers. Considering that effects of food restriction is opposite between before and after birth, we further searched genes which are regulated oppositely against adult calorie restriction and commonly against aging. Searched genes were included in groups related to the immune system, obesity and heart disease. Among these genes, trib1 has already been demonstrated to contribute to an increased risk of cardiovascular disease. The present result suggests that trib1 is a target of DOHaD. In addition, lepr was also dow-regulaed by maternal FR, suggested a potential role of this gene in induction of obesity. Promotor DNA methylation profiling as well as gene expression profiling revealed glucocorticoid target genes were regulated by maternal FR, supported previous reports suggesting important role of glucocorticoid in DOHaD.
2013-08-20 | GSE49964 | GEO
Project description:A large number of rodent studies have supported the developmental origins of health and disease (DOHaD) hypothesis that interauterine undernutrition (IU) is a risk factor for non-communicable diseases. The effect of IU is considered to be induced thorough epigenetic programming in the fetal tissues. We have recently carried out global transcriptome expression and promoter DNA methylation analyses on the fetal mouse liver following maternal 50% food restriction (FR) during late gestation, and reported a list of fetal liver genes that were transcriptionally or epigenetically regulated by IU (Ogawa et al., 2014, Congenital Anomalies). We have already reported the genes that were regulated oppositely between maternal and fetal livers (Ogawa et al., 2014, Congenital Anomalies). Here, we considered that the fetal liver is a hematopoietic organ, and exposed nine-week-old male mice (C57BL/6J from Japan SLC, Hamamatsu, Japan; n=8 / group) to 50% FR (chow; CE-2, CLEA, Tokyo Japan) for two weeks and carried out global gene expression analysis on the whole blood by a method reported previously (Ogawa et al., 2014, Congenital Anomalies).
2016-03-03 | GSE78817 | GEO