Ontology highlight
ABSTRACT:
PROVIDER: PRJNA940272 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23680600_1.fastq.gz | Fastqsanger.gz | |||
| SRR23680600_2.fastq.gz | Fastqsanger.gz | |||
| SRR23680601_1.fastq.gz | Fastqsanger.gz | |||
| SRR23680601_2.fastq.gz | Fastqsanger.gz | |||
| SRR23680602_1.fastq.gz | Fastqsanger.gz |
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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
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 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). Male C57BL/6J mice at 9 weeks (Japan SLC, Hamamatsu, Japan ; n=8 / group) were exposed to 50% FR (chow; CE-2, CLEA, Tokyo Japan) for 2 weeks. After 2 weeks, the mice were anesthetized with somunopentyl®(Kyoritsu eiyaku, Tokyo) at a dose of 0.5 mL/kg, and blood was taken from the right ventricle of the heart. Blood samples were immediately immersed in liquid nitrogen and stored at -80°C. All animal care and experimental procedures were approved by the Institutional Animal Care and Use Committee of Showa University, and caried out at animal facilities in Showa University. DNA Microarray analysis was carried out on 3 pools, respectively. Pool 1 included samples from animal No. 1-8 in each group (control and 50% FR). Pool 2 included samples from animal No. 1-4 in each group. Pool 3 included samples from animal No. 5-8 in each group.
2016-03-03 | E-GEOD-78817 | biostudies-arrayexpress
Project description:Proteome profiling was performed to investigate changes at a molecular level in the mouse corneal endothelium (CE) along with the basement membrane exposed to cigarette smoke (CS). Pregnant mice (gestation days 18-20) were placed in a whole-body exposure smoking chamber and a few days later pups were born. After 3½ months of CS exposure, the Confoscan4 scanning microscope was used to examine the CE of CS-exposed and control (Ct) mice. The CE was peeled under a microscope and maintained as four biological replicates (two male and two female) for CS-exposed and Ct mice; each replicate consisted of 16 CE. The proteome of the CE was investigated through mass-spectrometry using 8-plex isobaric tandem mass tags (TMT). The CE images of CS-exposed and Ct mice revealed a difference in the shape of corneal endothelial cells (CECs) accompanied by a nearly 10% decrease in CEC density (p = 3.0e-0.5) resulting from exposure to CS. The proteome profiling identified a total of 524 proteins exhibiting statistically significant changes in CE from CS-exposed and Ct mice. Importantly, proteins known to be an integral part of the basement membrane including COL4α1, COL4α2, COL4α3, COL4α4, COL4α5, and COL4α6, Col8α1, Col8α2, FN1, etc. exhibited diminished protein levels in the CE of CS-exposed mice. Here, we report the effects of CS on the CE, and our data strongly suggest that CS exposure results in reduced CEC density and diminished concentration of proteins known to be an integral part of the basement membrane.
2021-09-09 | PXD020036 | Pride
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. C57BL/6J mice were purchased from Japan SLC Co. Ltd. (Hamamatsu, Japan). The animals were housed at the Animal Institution in Showa University. They were maintained in cages in a ventilated animal room with controlled temperature and relative humidity with a 12 h light: 12 h dark schedule (lights turned on at 8:00 AM) and had access to chow (CE-2, CLEA Japan) and tap water ad libitum. As per the supplier’s (CLEA) information, CE-2 includes 51.4% nitrogen free extracts, 24.9% crude protein, 8.6% moisture, 6.7% crude ash, 4.6% crude fat, and 3.7% crude fiber. The physiological fuel value is 346.7 kcal per 100 g chow. All animal experiments were started after a period of acclimation of at least one week. Pregnant animals were obtained by housing females with males (1-2 females/male). The day the vaginal plug was observed was designated embryonic day 0 (ED0) and gestation day 0 (GD0). 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 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 were carefully removed avoiding any other tissues contamination. The liver was collected from six mothers in each group. Fetal liver was collected from two male fetuses from each mother. The liver was also collected from mothers to compare with fetal one in gene expression analysis. The harvested livers were immediately immersed in liquid nitrogen (N2) and stored at -80ºC. In all combinations, total RNA (1000 ng) was labeled with either Cy3 or Cy5 dye using an Agilent Low RNA Input Fluorescent Linear Amplification Kit (Agilent Technologies Inc., CA, USA). Fluorescently labeled targets of control as well as treated samples were hybridized to the same microarray slide with 60-mer probes (4 x 44K (41,090 gene probes), mouse whole genome, Agilent). A flip labelling (dye-swap or reverse labelling with Cy3 and Cy5 dyes) procedure was followed to nullify the dye bias associated with unequal incorporation of the two Cy dyes into cDNA. Hybridization and wash processes were performed according to the manufacturer’s instructions, and hybridized microarrays were scanned using an Agilent Microarray scanner. For the detection of significantly differentially expressed genes between control and exercise samples each slide image was processed by Agilent Feature Extraction software (version 9.5.3.1).
2013-08-20 | E-GEOD-49964 | biostudies-arrayexpress
Project description:The knowledge of the genetic architecture behind feed efficiency would allow to breed more efficient animals maximizing farm profitability and reducing the environmental impact of animal production. This study analyzes high throughput gene expression data from milk samples to determine key genes and biological mechanisms associated to feed efficiency in dairy sheep.A detailed description of the sheep management practices and calculations for the feed efficiency index (FEI) are detailed in 10.3168/jds.2020-19061. For these analyses, we selected animals with divergent FEI values from a group of 40 lactating Assaf ewes. RNA-Seq was performed on milk somatic cell samples from 8 high feed efficiency sheep (H-FE), FEI = −0.29 (SD = 0.23), RFI = −0.16 (SD = 0.25), and 8 low feed efficiency sheep (L-FE), FEI = 0.81 (SD = 0.24), RFI = 0.19 (SD = 0.24)).
2023-02-14 | E-MTAB-12355 | biostudies-arrayexpress
Project description:To better understand the hepatic metabolic response to intermittent fasting in chickens, Red Junglefowl chickens were raised on ad libitum (AL) feed until 14 days of age and then kept on AL feeding, switched to chronic feed restriction (CR) to around 70% or switched to an intermittent fasting (IF) regimen consisting of two fed days (150% of age-matched weight-specific AL intake offered daily) followed by a non-fed day. AL and CR were culled at 36 days of age, and IF birds either at 40 days of age (second consecutive feeding day) or 41 days of age (fasting day).
2022-04-14 | E-MTAB-7829 | biostudies-arrayexpress
Project description:Objective: Although relationships between smoking and cardiovascular diseases (CVD), and CVD and lipids are established, direct impact of cigarette smoke (CS) on lipidomes remains elusive. We investigated the effect of 6 month smoke exposure on a well-established mouse model for human atherogenesis, Apoe mouse plasma, liver, and aorta molecular lipid profiles and liver transcriptome. // Methods: Plasma, liver, and aorta samples from Apoe mice exposed to CS or fresh air for 6 months were extracted for lipids using robotic-assisted method and analyzed by mass spectrometry. Gene expression of samples from the same livers was obtained on microarrays. Development of atherosclerosis in aorta was further assessed by plaque size measurement in the aortic arch and lipoprotein measurements in plasma and in the plaque. // Results: CS increased most lipid classes and molecular lipid species in tissues evaluated. In plasma, free cholesterol, ceramides, cerebrosides, and majority of phospholipids were increased in CS-exposed mice. In liver, CS elevated several lipid species including free and esterified cholesterol, triacylglycerols, phospholipids, sphingomyelins, and ceramides. In aorta, more than 2-fold higher cholesteryl ester (CE), lysophosphatidylcholine, and glucosyl/galactosylceramide levels were recorded in mice exposed to CS compared to mice exposed to fresh air. Moreover, CS exposure induced a significant decrease in several plasma CE and phosphatidylcholine species that contained polyunsaturated fatty acids. Genes involved in amino acid and lipid metabolism showed perturbed transcription profiles in liver. // Conclusion: These data reveal molecular details accompanying the increase in plaque size, sign of atherogenesis in Apoe mice, which is accelerated by CS exposure.
2013-10-03 | E-MTAB-1195 | biostudies-arrayexpress