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Omics score: 18

Analysis of fetal livers from male mice after protein-restricted diet in mothers

ABSTRACT: Prenatal nutrition as influenced by nutritional status of the mother has been identified as a determinant of adult disease. Feeding low-protein diets during pregnancy in rodents is a well-established model to induce “programming” events in offspring. We hypothesized that protein restriction would influence fetal lipid metabolism by inducing epigenetic adaptations. Methodology/Principal Findings: Pregnant C57BL/6J OlaHsd mice were exposed to a protein restriction protocol (9% vs. 18% casein). Shortly before birth, dams and fetuses were sacrificed. To identify putative epigenetic changes, CpG island methylation microarrays were performed on DNA isolated from fetal livers. Overall design: 10 fetal livers: 5 mice from protein-restriction group (mice 1-5, labeled with Alexa 647) and 5 mice from control group (mice 6-10, labeled with Alexa 555). 5 arrays were used for the mice combinations 1/6, 2/7, 3/8, 4/9, 5/10. All arrays were run at the UHN Microarray Centre, Toronto.

INSTRUMENT(S): MCGI4.6Kv1_CPG_Mouse_Array_UMCG

ORGANISM(S): Mus musculus

SUBMITTER: vincent bloks

PROVIDER: GSE15280 | GEO | 2009-11-03

SECONDARY ACCESSION(S): PRJNA116505

REPOSITORIES: GEO

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Analysis of fetal livers from male mice after protein-restricted diet in mothers

Project description:Prenatal nutrition as influenced by nutritional status of the mother has been identified as a determinant of adult disease. Feeding low-protein diets during pregnancy in rodents is a well-established model to induce “programming” events in offspring. We hypothesized that protein restriction would influence fetal lipid metabolism by inducing epigenetic adaptations. Methodology/Principal Findings: Pregnant C57BL/6J OlaHsd mice were exposed to a protein restriction protocol (9% vs. 18% casein). Shortly before birth, dams and fetuses were sacrificed. To identify putative epigenetic changes, CpG island methylation microarrays were performed on DNA isolated from fetal livers. 10 fetal livers: 5 mice from protein-restriction group (mice 1-5, labeled with alexa 647) and 5 mice from control group (mice 6-10, labeled with alexa 555). 5 arrays were used for the mice combinations 1/6, 2/7, 3/8, 4/9, 5/10. All arrays were run at the UHN Microarray Centre, Toronto.

2014-05-01 | E-GEOD-15280 | ArrayExpress

Rat liver ESI-MS/MS

Project description:one-carbon metabolism in the liver plays a critical role in placental and fetal growth. Impaired functioning of one-carbon metabolism is associated with increased homocysteine (Hcy) levels. In this study, we applied a comprehensive proteomic approach to identify differential expression of proteins related to one-carbon metabolism in the livers of rat offspring as an effect of maternal food restriction during gestation. We determined that betaine-homocysteine S-methyltransferase 1 (BHMT1), methylenetetrahydrofolate dehydrogenase 1 (MTHFD1), and ATP synthase subunit beta mitochondrial (ATP5B) expression levels were significantly reduced in the livers of rat offspring exposed to maternal food restriction during gestation compared with in the offspring of rats fed a normal diet (p<0.05).

2015-09-07 | PXD002578 | Pride

mRNA expression in Zfp36L2 knockout E14.5 fetal liver

Project description:ZFP36L2, zinc finger protein 36, C3H type-like 2 (also known as Brf2, Erf2, Tis11D) is a member of the tristetraprolin (TTP; Zfp36) family of tandem CCCH zinc finger proteins that can bind to AU-rich elements (AREs) in the 3'-untranslated region of mRNAs, leading to their deadenylation and subsequent degradation. We have generated Zfp36l2 knockout mice. Knockout mice were born at the expected Mendelian frequency, but within several weeks of birth they died rather suddenly with pallor and frequent intestinal hemorrhage. These mice exhibited pancytopenia, decreased hematopoietic progenitor cells from fetal liver and yolk sac, and ineffective hematopoietic stem cells. Since ZFP26L2 is likely to function as an ARE-containing mRNA destabilizing protein, we were interested in identifying any abnormally stabilized transcripts in fetal livers from the Zfp36l2 knockout mice whose protein product may directly or indirectly affect hematopoietic stem cell function. Overall design: Total RNA was isolated from individual embryonic day 14.5 fetal livers. Five wild type and five knockout fetal livers were used to generate 5 wild type replicates and 5 knockout replicates. RNA expression from knockout fetal livers was compared to wild type fetal livers.

2009-08-06 | GSE15146 | GEO

Paternally-induced transgenerational environmental reprogramming of metabolic gene expression in mammals (meDIP)

Project description:Epigenetic information can be inherited through the mammalian germline, and represents a plausible transgenerational carrier of environmental information. To test whether transgenerational inheritance of environmental information occurs in mammals, we carried out an expression profiling screen for genes in mice that responded to paternal diet. As part of this analysis, we chracterise the changes in sperm cytosine methylation in response to different diets. Characterizing the RNA exression changes in livers of offspring mice in response to the paternal diet, comparing between low-protein diet and control-diet. Examination the effect of 3 different paternal diets, control diet, Caloric Restriction and low-protein diet, on sperm cytosine methylation.

2014-05-02 | E-GEOD-25898 | ArrayExpress

Paternally-induced transgenerational environmental reprogramming of metabolic gene expression in mammals (meDIP)

Project description:Epigenetic information can be inherited through the mammalian germline, and represents a plausible transgenerational carrier of environmental information. To test whether transgenerational inheritance of environmental information occurs in mammals, we carried out an expression profiling screen for genes in mice that responded to paternal diet. As part of this analysis, we chracterise the changes in sperm cytosine methylation in response to different diets. Characterizing the RNA exression changes in livers of offspring mice in response to the paternal diet, comparing between low-protein diet and control-diet. Overall design: Examination the effect of 3 different paternal diets, control diet, Caloric Restriction and low-protein diet, on sperm cytosine methylation.

2011-01-14 | GSE25898 | GEO

Expression profiles of TIS21/BTG2/PC3 gene knockout in liver of C57BL/6J mice in response to starvation

Project description:TIS21/BTG2/PC3 has been known as one of the primary response genes regulated by p53-dependent and p53-independent manners. In our study, TIS21 reveals various functions as a tumor suppressor in human and mouse tumors. Recently, it has been reported that expression of TIS21 can be induced during starvation in liver, muscle and white adipose tissues. However, there was no report on the role of TIS21 in response to starvation. To investigate any role of TIS21 gene in the metabolic stimulation, we fasted C57BL/6J mice for overnight (20 hour), and then transcriptional profiles of the TIS21-knockout and TIS21-wild type mice were compared. Along with this trial, we also analyzed transcriptional profiles of fetal livers of the 13.5 day-old embryos derived from the TIS21-wild type and knockout mice. Overall design: TIS21-KO vs. TIS21-WT from the livers of the 10 week-old male mice starved for 20 hour (from 5:00pm to next day 1:00 pm), and the fetal livers of the 13.5 days old embryos. The mRNAs isolated from fetal livers were pooled (n>3). Biological samples: mRNAs isolated from livers of the TIS21-KO adult mice (KO-Ad) vs. livers of the TIS21 wild-type adult mice (WT-Ad); pooled mRNAs from livers of TIS21-KO embryos (KO-Fetal) vs. pooled mRNAs from livers of wild-type fetal embryos (WT-Fetal); Per each sample, the transcriptional profile was measured in technical duplication.

| GSE105772 | GEO

Restricted Feeding Reveals Maternal Entrainment of Weak Circadian Oscillators in Fetal Mouse Livers

Project description:Although circadian clocks oscillate in most cells, it has been difficult to detect canonical expression of clock genes in fetal rodent tissues, including the fetal liver. The oscillation status of fetal clocks and the maternal influence on these clocks have not yet been conclusively defined. Here we report that, when the mother mice are under restricted feeding, the expression rhythms of several clock genes can be detected in fetal mouse livers. Those rhythms, although of low amplitude, reversed their profiles under opposite feeding cycles, suggesting maternal entrainment of the weak fetal liver clocks. However, Bmal1 could show biphasic expression in the fetal livers. The expression of some metabolic genes (e.g. Insig1) also showed biphasic daily changes in fetal livers, possibly as a result of interactions between the unique in utero milieu and the fetal liver clocks. Regular rhythms of clock gene expression were detected in dissociated fetal hepatocytes in culture. Differential expression of metabolic genes were found between fetal and adult livers, suggesting that metabolic features affected clock amplitude. Genome-wide differences in DNA methylation were also found between adult and fetal livers. Some of those epigenetic changes were likely critical for the developmental changes in clock amplitudes. Overall design: The whole genome methylation status of two samples (Fetal and Adult) were analysed by reduced representational bisulfite sequencing (RRBS)

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Ontogeny, distribution and potential roles of hydroxymethylcytosine in human liver function

Project description:Background: Interindividual differences in liver functions such as protein synthesis, lipid and carbohydrate metabolism and drug metabolism are influenced by epigenetic factors. The role of the epigenetic machinery in such processes has, however, been barely investigated. 5-hydroxymethylcytosine (5hmC) is a recently re-discovered epigenetic DNA modification that plays an important role in the control of gene expression. Results: In this study, we investigate 5hmC occurrence and genomic distribution in 8 fetal and 7 adult human liver samples in relation to ontogeny and function. LC-MS analysis shows that in the adult liver samples 5hmc comprises up to 1% of the total cytosine content, whereas in all fetal livers it is below 0.125%. Immunohistostaining of liver sections with a polyclonal anti-5hmC antibody shows that 5hmC is detected in most of the hepatocytes. Genome-wide mapping of the distribution of 5hmC in human liver samples by next-generation sequencing shows significant differences between fetal and adult livers. In adult livers, 5hmC occupancy is overrepresented in genes involved in active catabolic and metabolic processes, whereas 5hmC elements which are found in genes exclusively in fetal livers and disappear in the adult state, are more specific to pathways for differentiation and development. Conclusions: Our findings suggest that 5-hydroxymethylcytosine plays an important role in the development and function of the human liver and might be an important determinant for development of liver diseases as well as of the interindividual differences in drug metabolism and toxicity. 8 fetal and 7 adult human liver samples

2014-05-03 | E-GEOD-49291 | ArrayExpress

Mus musculus

Project description:Analysis of fetal livers from male mice after protein-restricted diet in mothers

| PRJNA116505 | ENA

Postnatal Growth Restriction and Gene Expression Changes in a Mouse Model of Fetal Alcohol Syndrome (Liver)

Project description:Growth restriction, craniofacial dysmorphology and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal and/or postnatal, but the underlying mechanisms remain unknown. We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome, e.g. craniofacial changes and growth restriction in adolescent mice. Here we further characterize the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of non-fostered ethanol-exposed and control mice at postnatal day 28. We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiological result of ethanol exposure in utero. We also find that, despite some catch-up growth after five weeks of age, the effect extends into adulthood, consistent with longitudinal studies in humans. Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis and lipid metabolism. Gene expression changes in the livers of offspring exposed to alcohol in utero compared to controls.

2012-06-26 | E-GEOD-23106 | ArrayExpress

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