Project description:This dataset was generated with the goal of comparative study of gene expression in three brain regions and two non-neural tissues of humans, chimpanzees, macaque monkeys and mice. Using this dataset, we performed studies of gene expression and gene splicing evolution across species and search of tissue-specific gene expression and splicing patterns. We also used the gene expression information of genes encoding metabolic enzymes in this dataset to support a larger comparative study of metabolome evolution in the same set of tissues and species. 120 tissue samples of prefrontal cortex (PFC), primary visual cortex (VC), cerebellar cortex (CBC), kidney and skeletal muscle of humans, chimpanzees, macaques and mice. The data accompanies a large set of metabolite measurements of the same tissue samples. Enzyme expression was used to validate metabolite measurement variation among species.
Project description:This dataset was generated with the goal of comparative study of gene expression in three brain regions and two non-neural tissues of humans, chimpanzees, macaque monkeys and mice. Using this dataset, we performed studies of gene expression and gene splicing evolution across species and search of tissue-specific gene expression and splicing patterns. We also used the gene expression information of genes encoding metabolic enzymes in this dataset to support a larger comparative study of metabolome evolution in the same set of tissues and species.
Project description:Inhibitors of glucose (IO+DHEA group) or fatty acids (ETOMOXIR group) metabolism were applied during bovine oocyte in vitro maturation (IVM). Control group was conducted in standard maturation conditions. In vitro fertilization and embryo culture were applied. Obtained blastocysts were analysed with regard to lipidome, metabolome (mass spectrometry), transcriptome (RNA Seq) and lipid droplets staining (BODIPY).
Project description:Resolution of infection results in development of trained innate immunity which is typically beneficial for the host in defense against unrelated secondary infection. Epigenetic changes underlie the establishment of trained innate immunity therefore host metabolism and this response are intimately linked. However, little is known regarding the influence of lipids on the development and function of trained immunity. Utilizing two models of pulmonary bacterial infection combined with multi-omic approaches, we identified persistent, pathogen-specific changes to the lung lipidome that correlated with differences in the trained immune response. Further, we establish the specific cellular populations in the lung that contribute to this altered lipidome. Together these results expand our understanding of the pulmonary trained innate immune response and the contributions of host lipids in informing that response.
Project description:Microglia are specialized immune cells in the brain that eliminate misfolded protein deposits and cellular debris by phagocytosis. In Alzheimers disease, microglia clear the amyloid beta aggregates during disease onset but are unable to phagocytose them from the tissue environment during the late stages of the disease contributing to chronic inflammation. Lipids and metabolites orchestrate critical regulation events within the cell or by their secretion into the cellular microenvironment, yet, the effect of abeta on microglial lipidome and metabolome has not been well characterized till date. In this study, we used Multiple-Reaction Monitoring (MRM)-profiling to evaluate, for the first time, the lipid and metabolite changes in abeta-activated microglia that were isolated from mouse brains over 24 hours. We also developed a new bioinformatics pipeline to identify the statistically significant lipids and metabolites in abeta-treated microglial cells and condition medium that were differentially regulated compared to the vehicle controls. Triacylglycerides and phosphatidylglycerols were the most abundant lipid classes, whereas long-chain free fatty acids with 26 to 30 acyl chain carbon atoms were consistently decreased with abeta-treatment over time. Further, 42 significant metabolites were identified in cells. L-2-aminobutyric acid, hydroxybutyric acid, inosine, alanine, etc. were differentially regulated with abeta treatment suggesting changes in alanine, aspartate and glutamate metabolism, and arginine biosynthesis pathways. Selected metabolites were identified in the microglial conditioned medium, including stearic acid, tryptophan, palmitic acid, etc. that have been shown to affect the phagocytic properties of peripheral macrophages and may also play a role in the microglial phagocytic response. Thus, characterizing the lipidome and metabolome of microglia due to abeta identifies critical molecules involved in their immune response and highlight the molecular mechanisms of phagocytic function as well as dysfunction associated with AD.