Project description:Hippocampal tissues from 3xTg-AD mice treated with a CK1δ/ε inhibitor or vehicle, and non-transgenic mice treated with vehicle, were harvested and processed for proteomic analysis using label-free quantification.
Project description:Using RNA sequencing, we perform gene expression profile of five male mice treated with vehicle and five male mice sub-chronically treated with AM6545 at a dose of 1 mg/kg. To evaluate hippocampal modifications promoted by peripheral CB1R modulation, we analyze at transcript level hippocampal synaptoneurosomes fractions. This analysis revealed changes in the transcript usage of N-methyl-D-aspartate (NMDA) receptor 1 isoforms in AM6545 treated mice compared with vehicle-treated ones.
Project description:We found that a klotho protein fragment (KL-F), administered peripherally, induced cognitive enhancement and neural resilience. Here we report a proteomic analysis of whole hippocampal homogenates from mice treated with vehicle or KL-F (10 µg/kg, i.p.) four hours prior to exploration in the small Y-maze. The proteomic results showed glutamate receptor signaling as the top enriched canonical pathway by Ingenuity Pathway Analysis.
Project description:In this study, we determined the effect of chronic consistent hypoxia (CCH) and chronic intermittent hypoxia (CIH) on global gene expression in cortical and hippocampal region of developing mouse brain using long-oligo beadschip arrays. Keywords: Gene expression profile Control-Cortex: Cortical samples from 16 days old mice were analysed on whole-genome expression chips to reveal expression profile at this developmental stage. Used as control for Chronic Hypoxia Treated cortical samples. CCH-Cortex: Cortical samples from 2-week CCH treated mice were analysed on whole-genome expression chips to reveal the changes in gene expression profile following 2-week CCH treatment. CIH-Cortex: Cortical samples from 2-week CCH treated mice were analysed on whole-genome expression chips to reveal the changes in gene expression profile following 2-week CIH treatment. Control-Hippocampus: Hippocampal samples from 16 days old mice were analysed on whole-genome expression chips to reveal expression profile at this developmental stage. Used as control for Chronic Hypoxia Treated hippocampal samples. CCH-Hippocampus: Hippocampal samples from 2-week CCH treated mice were analysed on whole-genome expression chips to reveal the changes in gene expression following 2-week CCH treatment. CIH-Hippocampus: Hippocampal samples from 2-week CCH treated mice were analysed on whole-genome expression chips to reveal the changes in gene expression following 2-week CIH treatment.
Project description:Small RNA sequencing data (TruSeq small RNA library preparation kit v2) from serum samples and tumor tissue of orthotopically injected mice (SH-SY5Y cell line) and unengrafted mice, treated with idasanutlin, temsirolimus and vehicle control.
Project description:Histone deacetylase inhibitors (HDACis) have been shown to potentiate hippocampal-dependent memory and synaptic plasticity and to ameliorate cognitive deficits and degeneration in animal models for different neuropsychiatric conditions. However, the impact of these drugs on hippocampal histone acetylation and gene expression profiles at the genomic level, and the molecular mechanisms that underlie their specificity and beneficial effects in neural tissue, remains obscure. Here, we mapped four relevant histone marks (H3K4me3, AcH3K9,14, AcH4K12 and pan-AcH2B) in hippocampal chromatin and investigated at the whole-genome level the impact of HDAC inhibition on acetylation profiles and basal and activity-driven gene expression. HDAC inhibition caused a dramatic histone hyperacetylation that was largely restricted to active loci pre-marked with H3K4me3 and AcH3K9,14. In addition, the comparison of Chromatin immunoprecipitation sequencing and gene expression profiles indicated that Trichostatin A-induced histone hyperacetylation, like histone hypoacetylation induced by histone acetyltransferase deficiency, had a modest impact on hippocampal gene expression and did not affect the transient transcriptional response to novelty exposure. However, HDAC inhibition caused the rapid induction of a homeostatic gene program related to chromatin deacetylation. These results illuminate both the relationship between hippocampal gene expression and histone acetylation and the mechanism of action of these important neuropsychiatric drugs. Examination of 4 different histone modifications in the hippocampus of vehicle (DMSO/Saline) or HDACi TSA (2.4 mg/kg)-treated mice. Samples were obtained 30 min after intraperitoneal administration of either TSA or Vehicle. NOTE: The ChIPseq experiments described here and those presented in the series GSE44854 were performed in paralell. Therefore, some control samples are part of both datasets (GSM1062434, GSM1062437, GSM1062441 and GSM1062442).