Effect of estradiol on murine alveolar macrophages and RAW264.7 cells in vitro
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ABSTRACT: Mouse BAL alveolar macrophages from pregnant E14 and control dams are compared to RAW cells cultured with estradiol to determine shared gene expression change patterns induced by pregnancy and estrogen BAL cells from intact pregnant and control mice were directly processed for RNA extraction. RAW cells were cultured overnight with estradiol or vehicle, then RNA was exctracted.
Project description:Mouse BAL alveolar macrophages from pregnant E14 and control dams are compared to RAW cells cultured with estradiol to determine shared gene expression change patterns induced by pregnancy and estrogen
Project description:Maternal exposures during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. We investigated whether feeding pregnant rats a high fat (HF) or ethinyl-estradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. Here we show that mammary tumorigenesis is higher in daughters and granddaughters of HF rat dams and in daughters, granddaughters and great-granddaughters of EE2 rat dams. Outcross experiments indicate that increased mammary cancer risk is transmitted to HF granddaughters equally through the female or male germlines, but it is only transmitted to EE2 granddaughters through the female germline. The effects of maternal EE2 exposure on offspring's mammary cancer risk are associated with alternations in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and estrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through non-genetic means
Project description:Maternal exposures during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. We investigated whether feeding pregnant rats a high fat (HF) or ethinyl-estradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. Here we show that mammary tumorigenesis is higher in daughters and granddaughters of HF rat dams and in daughters, granddaughters and great-granddaughters of EE2 rat dams. Outcross experiments indicate that increased mammary cancer risk is transmitted to HF granddaughters equally through the female or male germlines, but it is only transmitted to EE2 granddaughters through the female germline. The effects of maternal EE2 exposure on offspring's mammary cancer risk are associated with alternations in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and estrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through non-genetic means We examined the whole genome methylation status of both control and EE2-supplemented diet rats in three consecutive generations
Project description:DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours, compared to control cells.
Project description:Scarcity of gender specific donor hearts highlights the importance of mesenchymal stem cells (MSCs) as a therapeutic tool for heart repair. However, inefficient incorporation, retention, and activity of MSCs in cardiac tissue remains an obstacle. Since surge in follicular estradiol (μmolar-range) triggers tissue remodeling (e.g. ovulation) and estradiol exerts beneficial actions on the cardiovascular system, we hypothesized that estradiol may promote/improve MSC-mediated cardiac repair processes. Methods: Wharton’s jelly-derived MSCs were used, to assess the effects of estradiol on their proliferation, directed-migration and engraftment in murine heart slices, ex vivo. Results: MSCs expressed estrogen receptors (ERs) α and β, and estradiol promoted MSC proliferation (measured using xCELLigence real-time cell-impedance system and DNA-quantification). Estradiol up-regulated mRNA (qRT-PCR) and protein expression (western blotting) of ERα, ERβ, EMMPRIN, and MMP-9, yet down-regulated MMP-2 expression. In MSCs estradiol, up-regulated mRNA expression of VEGF-A, VCAM-1, and angiogenin, and stimulated NO production via ER. Proteomic analysis revealed that in MSCs estradiol up-regulated 47 proteins, down-regulated 7 proteins, and increased the expression of key biochemical components/pathways involved in tissue repair. In MSCs co-cultured with murine heart-slices, estradiol significantly induced MSC migration in an ER-dependent fashion (and preferentially via ERα) and significantly increased the secretion of MMP-2, MMP-9, angiogenin and VEGF. Conclusion: Estradiol facilitates the integration/engraftment of MSCs into heart slices by promoting MSC proliferation and migration and these beneficial effects are mediated via increases in molecules/pathways involved in tissue remodeling and angiogenesis. Priming of MSCs with estradiol may enhance their ability to repair/regenerate cardiac tissue in women.
Project description:DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical artery endothelial cells (HUAECs) exposed to 1 nmol/L estradiol and/or 100 µg/ml oxidized low density lipoprotein (oxLDL) for 24 hours compared to control cells.
Project description:Lysozyme-GFP ER-HoxA9 cells were cultured in the presence of estradiol (active ER-HoxA9) or in the absence of estradiol (inactive ER-HoxA9). Samples were taken at 10 time points over a 120 hour time course of myeloid differentiation to examine those gene expression changes that accompany differentiation upon the release of HoxA9 differentiation arrest.
Project description:Pregnant mice (Dams) were exposed to cigarette smoke or filtered air. Lung tissue and RNA were harvested from the lungs of the Dams and their offspring and underwent transcriptomic analysis.
Project description:Analysis of gene expression in the pituitary gland of pregnant versus non-pregnant dams. We describe the dynamic control of pituitary gene expression in the pregnant mother, with implications for the regulation of maternal metabolic adaptations to pregnancy.
Project description:Effect of an immunosupressive dose of TCDD, a ligand for the aryl hydrocarbon receptor, on the gene expression profile of fetal DN thymocytes and thymic emigrants C57BL6 mice were mated and the pregnant dams sacrifice at day 15 of gestation. Fetal thymic lobes were prepared and cultured for 6 days on culture inserts (5-6 lobes/culture insert). Medium, containing either 10 nM TCDD or solvent control was exchanged every 48 hours. At day six (gestation day 21, corresponding to birth), single cell suspensions of the thymocytes were prepared and CD4-CD8- cells isolated by MACS sorting. Purity of the population was checked FACS analysis, to be greater 95%. RNA was purified (TRIZOL), amplified (Ambion Kit) and processed (Affymetrix standard protocol) according to manufacturers instructions. Raw cell files were processed with the bioconductor affy package