Osteocalcin of maternal and embryonic origins synergize to establish homeostasis in offspring
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1042824 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26881325_1.fastq.gz | Fastqsanger.gz | |||
| SRR26881325_2.fastq.gz | Fastqsanger.gz | |||
| SRR26881326_1.fastq.gz | Fastqsanger.gz | |||
| SRR26881326_2.fastq.gz | Fastqsanger.gz | |||
| SRR26881327_1.fastq.gz | Fastqsanger.gz |
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Project description:Many physiological functions regulated by osteocalcin are affected in adult offspring of mothers experiencing an unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together these observations suggest that osteocalcin functions during pregnancy may be a broader determinant of organismal homeostasis in adult mammals than previously thought. To test this hypothesis, we analyzed in unchallenged wildtype and Osteocalcin-deficient, newborn, and adult mice of various genotypes and origin, and that were maintained on different genetic backgrounds, the functions of osteocalcin in the pancreas, liver and testes and their molecular underpinnings. This analysis revealed that providing mothers are themselves Osteocalcin-deficient, Osteocalcin haploinsufficiency in embryos hampers insulin secretion, liver gluconeogenesis, glucose homeostasis, testes steroidogenesis in adult offspring; inhibits cell proliferation in developing pancreatic islets and testes; and disrupts distinct programs of gene expression in these organs and in the brain. This study indicates that provided mothers lack an allele, osteocalcin exerts dominant functions. Furthermore, through their synergistic regulation of multiple physiological functions, osteocalcin of maternal and embryonic origins contributes to the establishment and maintenance of organismal homeostasis in newborn and adult offspring.
2023-11-24 | GSE248211 | GEO
Project description:Many physiological osteocalcin-regulated functions are affected in adult offspring of mothers experiencing unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together these observations suggest that osteocalcin may broadly function during pregnancy to determine organismal homeostasis in adult mammals. To test this hypothesis, we analyzed in unchallenged wildtype and Osteocalcin-deficient, newborn and adult mice of various genotypes and origin maintained on different genetic backgrounds, the functions of osteocalcin in the pancreas, liver and testes and their molecular underpinnings. This analysis revealed that providing mothers are Osteocalcin-deficient, Osteocalcin haploinsufficiency in embryos hampers insulin secretion, liver gluconeogenesis, glucose homeostasis, testes steroidogenesis in adult offspring; inhibits cell proliferation in developing pancreatic islets and testes; and disrupts distinct programs of gene expression in these organs and in the brain. This study indicates that osteocalcin exerts dominant functions in most organs it targets. Furthermore, through their synergistic regulation of multiple physiological functions, osteocalcin of maternal and embryonic origins contributes to the establishment and maintenance of organismal homeostasis in newborn and adult offspring.
| S-SCDT-10_1038-S44319-023-00031-3 | biostudies-other
Project description:Many physiological osteocalcin-regulated functions are affected in adult offspring of mothers experiencing unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together these observations suggest that osteocalcin may broadly function during pregnancy to determine organismal homeostasis in adult mammals. To test this hypothesis, we analyzed in unchallenged wildtype and Osteocalcin-deficient, newborn and adult mice of various genotypes and origin maintained on different genetic backgrounds, the functions of osteocalcin in the pancreas, liver and testes and their molecular underpinnings. This analysis revealed that providing mothers are Osteocalcin-deficient, Osteocalcin haploinsufficiency in embryos hampers insulin secretion, liver gluconeogenesis, glucose homeostasis, testes steroidogenesis in adult offspring; inhibits cell proliferation in developing pancreatic islets and testes; and disrupts distinct programs of gene expression in these organs and in the brain. This study indicates that osteocalcin exerts dominant functions in most organs it influences. Furthermore, through their synergistic regulation of multiple physiological functions, osteocalcin of maternal and embryonic origins contributes to the establishment and maintenance of organismal homeostasis in newborn and adult offspring.
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Project description:Pregnant rats were received i.p. injection of L‑NAME (250 mg/kg/day) from gestational day 15 to 20 to establish preeclampsia model. Proteome analysis of cerebrospinal fluid on postnatal day 5 were performed on male offspring.
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Project description:This SuperSeries is composed of the following subset Series: GSE40471: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen expression) GSE40477: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen methylation) GSE40478: Maternal slimming reprograms metabolic gene expression in mice offspring (mRNA-Seq) Refer to individual Series
2012-08-30 | E-GEOD-40479 | biostudies-arrayexpress
Project description:Maternal overnutrition affects offspring susceptibility to nonalcoholic steatohepatitis (NASH). Male offspring from high-fat diet (HFD)-fed dams developed a severe form of NASH, leading to highly vascular tumor formation. The cancer/testis antigen HORMA domain containing protein 1 (HORMAD1), one of 146 upregulated differentially expressed genes in fetal livers from HFD-fed dams, was overexpressed with hypoxia-inducible factor 1 alpha (HIF-1alpha) in hepatoblasts and in NASH-based hepatocellular carcinoma (HCC) in offspring from HFD-fed dams at 15 weeks old. Hypoxia substantially increased Hormad1 expression in primary mouse hepatocytes. Despite the presence of three putative hypoxia response elements within the mouse Hormad1 gene, the Hif-1alpha siRNA only slightly decreased hypoxia-induced Hormad1 mRNA expression. In contrast, N-acetylcysteine, but not rotenone, inhibited hypoxia-induced Hormad1 expression, indicating its dependency on nonmitochondrial reactive oxygen species production. Synchrotron-based phase-contrast micro-CT of the fetuses from HFD-fed dams showed significant enlargement of the liver accompanied by a consistent size of the umbilical vein, which may cause hypoxia in the fetal liver. Based on these findings, a maternal HFD induces fetal origins of NASH/HCC via hypoxia, and HORMAD1 is a potential therapeutic target for NASH/HCC.
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Project description:Evaluate differences in gene methylation levels between offspring born after maternal bariatric surgery and their siblings born before surgery Offspring born after maternal bariatric surgery (AMS, N=25) vs. offspring born before maternal surgery (BMS, N=25)
2013-05-16 | E-GEOD-44798 | biostudies-arrayexpress
Project description:Evaluate differences in gene expression levels between offspring born after maternal bariatric surgery and their siblings born before surgery Offspring born after maternal bariatric surgery (AMS, N=23) vs. offspring born before maternal surgery (BMS, N=23)
2013-05-16 | E-GEOD-44407 | 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. 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.
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