Maternal immune activation (MIA) during pregnancy has been linked to an increased risk in the offspring to develop schizophrenia. In schizophrenic patients, a dysregulation of microglia, the brain''s immune competent cells, was reported and treatment with the immunomodulatory compound minocycline proved to be beneficial. Nevertheless, it remains unclear how specific minocycline treatment acts on microglia cells in vivo. Utilizing a mouse model of schizophrenia triggered by a maternal injection of the viral mimic PolyI:C we performed mRNA-sequencing on freshly isolated microglia form adult PolyI:C mice with and without chronic minocycline treatment. In the adult offspring an altered microglial transcriptome associated with changes in cell activation, motility, adhesion and phagocytosis was accompanied by behavioral deficits. Treatment with 3mg/kg/day minocycline for 5 weeks restored the changes in microglial transcriptional signature and phagocytic activity while attenuating the behavioral deficits. Our findings indicate that maternal immune activation induces profound changes in microglial transcriptome and function in the adult offspring and minocycline represents a valuable drug to restore a normal cellular and functional phenotype.
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Sex, Age, Specimen part, Disease, Cell line, Treatment
View Samplesmouse pancreatic beta cells were cultured in the presence glucose. RNA was extracted from cells and the transcriptome was profiled.
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View SamplesIn the semi-dominant mouse model, Nan (neonatal anemia), heterozygotes suffer hemolytic anemia at birth and throughout life due to a missense mutation (E339D) in transcription factor KLF1 (Krüppel-like factor 1; formerly EKLF, erythroid Krüppel-like factor) Here, we focus on erythropoiesis in the adult spleen. We performed RNAseq in flow-sorted spleen erythroid precursors from adult Nan and WT littermates rendered anemic by phlebotomy as a means to identify global transcriptome changes specific to the Nan KLF1 defect, as opposed to those characterizing anemia generally. We show that (1) expression variation in adult Nan spleen is driven primarily by cell maturation, (2) genotype influences on gene expression are most prominent in late stages of erythroid differentiation when Klf1 expression is highest, (3) Nan-KLF1 produces tissue-specific differential gene expression, and (4) suboptimal stress and basal erythropoiesis with increased reactive oxygen species (ROS) contribute to anemia in adult Nan mice.
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Sex, Specimen part, Cell line
View SamplesRNA-seq of Babesia microti isolates and rodent host
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View SamplesRNA-seq of Babesia microti isolates and rodent host
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View SamplesRNA-seq of Babesia microti isolates and rodent host
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View SamplesRNA-seq of Babesia microti isolates and rodent host
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View SamplesRNA-seq of Babesia microti isolates and rodent host
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View SamplesRNA-seq of Babesia microti isolates and rodent host
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