Ontology highlight
ABSTRACT:
PROVIDER: PRJNA134619 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE25482: Fetal programming of hepatic transcriptome in response to gestational dietary protein levels in the pig (AP data set) GSE25483: Fetal programming of hepatic transcriptome in response to gestational dietary protein levels in the pig (HP data set) Refer to individual Series
2011-11-30 | E-GEOD-25484 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE33737: Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [AP] GSE33738: Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [HP] GSE33739: Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [LP] Refer to individual Series
2012-09-05 | E-GEOD-33740 | biostudies-arrayexpress
Project description:Fetal programming of hepatic transcriptome in response to gestational low dietary protein levels in the pig
| PRJNA144761 | ENA
Project description:Fetal programming of hepatic transcriptome in response to gestational dietary protein levels in the pig (AP data set)
| PRJNA142599 | ENA
Project description:Fetal programming of hepatic transcriptome in response to gestational dietary protein levels in the pig (HP data set)
| PRJNA142601 | ENA
Project description:Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [HP]
| PRJNA154189 | ENA
Project description:Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [AP]
| PRJNA154365 | ENA
Project description:Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [LP]
| PRJNA154363 | ENA
Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.
2014-10-25 | E-GEOD-62715 | biostudies-arrayexpress