Project description:The oscillation status of the circadian clock during late gestation is not clear. To gain a better understanding on the oscillation state of the clock and possible influences by maternal cues, we performed transcriptome analyses on the fetal liver tissue during late gestation. Fetal liver transcriptome data were analyzed and compared to adult mouse data in the public database: GSE11923 and GSE13093 (only samples GSM327130 to GSM327141). Re-analyzed (gc-RMA) data from GSE11923 and GSE13093 linked below as supplementary files. Fetal mouse liver tissues were collected at four hours intervals across embryonic day 18 and day 19. Groups 1 and 2.
Project description:Using full-genome arrays, the expression of all XMEs was examined during fetal (gestation day (GD) 19), neonatal (postnatal day (PND) 7), prepubescent (PND30), middle age (12 mon), and old age (18 and 24 mon) in the C57Bl6/J mouse liver and compared to young adults. Fetal and neonatal life stages had a dramatic effect on XME expression compared to the relatively minor effects of old age. At all life stages except PND30 down-regulated genes outnumbered up-regulated genes. The altered XMEs included those in all of the major metabolic phases including phase I (alcohol and aldehyde dehydrogenase and Cyp genes), phase II (aldo-keto reductase, glutathione-S-transferases, sulfotransferases and UDP-glucuronosyl transferases) and phase III (transporters). We have generated a comprehensive catalog of XME hepatic gene changes through the life stages of the mouse that can be used to predict chemicals and chemical classes different life stages are more sensitive to. Some CEL files used in this study have been submitted through GSE21224. Keywords: gene expression/microarray We characterized gene expression changes in the developing mouse liver at gestational days (GD) 19), neonatal (postnatal day (PND) 7), prepubescent (PND30), middle age (12 mon), and old age (18 and 24 mon) in the C57Bl6/J mouse liver using full-genome microarrays and compared these changes to that in the adult liver.. We also compared results to GD19, PND32, and PND67 C3H mice. Total RNA was isolated from liver samples and gene expression analyzed using Affymetrix Mouse 430 2.0 GeneChips. Data from 28 samples, four mice in each of the age groups for C57BL/6 and C3H, were analyzed.
Project description:Alteration of kidney morphogenesis in diabetic pregnancies is poorly described, especially changes in the extracellular matrix (ECM) and glomerular basement membrane (GBM during glomerulogenesis. Addressing the ECM proteome, or matrisome, in the mouse fetal kidney in a healthy and diabetic environment will improve understanding about the association between ECM changes in the kidney as potential reprogramming mechanisms of kidney differentiation in diabetic pregnancies. Therefore, to better understand ECM composition and remodelling in kidney developmental and appreciate the alterations associated to the maternal diabetes, this project aimed to define the matrisome in the mouse fetal kidney on embryonic day 19. For this, we used an ECM enrichment approach combined with high resolution label-free tandem mass spectrometry to define the matrisome in the fetal mouse kidney (healthy and hyperglycemic) to test the hypothesis that maternal diabetes influences ECM composition, assembly and, therefore, biology.
Project description:Our strategy was to manipulate mTOR signaling in vivo, then characterize the transcriptome and translating mRNA in liver tissue. In adult rats, we used the non-proliferative growth model of refeeding after a period of fasting, and the proliferative model of liver regeneration following partial hepatectomy. We also studied livers from pre-term fetal rats (embryonic day 19-20) in which fetal hepatocytes are asynchronously proliferating. All three models employed rapamycin to inhibit mTOR signaling.
Project description:Using full-genome arrays, the expression of all XMEs was examined during fetal (gestation day (GD) 19), neonatal (postnatal day (PND) 7), prepubescent (PND30), middle age (12 mon), and old age (18 and 24 mon) in the C57Bl6/J mouse liver and compared to young adults. Fetal and neonatal life stages had a dramatic effect on XME expression compared to the relatively minor effects of old age. At all life stages except PND30 down-regulated genes outnumbered up-regulated genes. The altered XMEs included those in all of the major metabolic phases including phase I (alcohol and aldehyde dehydrogenase and Cyp genes), phase II (aldo-keto reductase, glutathione-S-transferases, sulfotransferases and UDP-glucuronosyl transferases) and phase III (transporters). We have generated a comprehensive catalog of XME hepatic gene changes through the life stages of the mouse that can be used to predict chemicals and chemical classes different life stages are more sensitive to. Some CEL files used in this study have been submitted through GSE21224. Keywords: gene expression/microarray
Project description:Various blood lineages, including lymphoid cells and myeloid cells, are produced from hematopoietic stem cells (HSCs) in the bone marrow. However, HSCs aren’t developed in the bone marrow during mouse embryogenesis. The first HSCs are found in the aorta-gonad-mesonephros region, the yolk sac, and the fetal liver, although the number is very few at embryonic day (E) 11. Most HSCs are observed in the fetal liver at E12. To understand the specific genes of nascent HSCs, we performed single-cell RNA-seq analysis of KIT-expressing cells sorted from the fetal liver at E12. We identified the nascent HSC population and found some feature genes in those cells. Therefore, our data will help us understand the nascent HSCs.
Project description:We employed marker-free single-cell RNA-Seq to characterize comprehensive transcriptional profiles of 52 EpCAM+ cells from postnatal day 3.25 mouse fetal livers. These cells show characters of cholangiocytes. Combined with our previous single cell data of E11.5~P2.5 mouse fetal livers, our data depict the dynamic trajectories with transcriptional profiles at single-cell resolution during mouse liver development, and provide insights into the fate decision and transcriptional control of self-renewal, differentiation and maturation of liver stem/progenitor cells.