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H3K9ac data from mouse models suggest structural changes in the murine brain epigenome that involve the nuclear lamina

ABSTRACT: To explore whether tau-related epigenomic changes that we found human brain H3K9ac data (Synapse ID: syn4896408) are recapitulated in mouse models known to accumulate tau, we generated hippocampal H3K9ac ChIP-seq profiles from two different mouse models each at an early and a late stage of neurodegeneration. Specifically, we studied 6 and 11 months old mutant tau mice (MAPT P301S), which start to accumulate phosphorylated tau in neurons by 6 months. Wild-type mice of the same age were used as controls. The second mouse model was the CK-p25 model, which is characterized by increased amyloid-β levels early after p25 induction followed by increased tau phosphorylation and neuronal loss at later stages. Three months old CK-p25 mice were studied 2 weeks and 6 weeks after p25 induction and compared with CK littermate controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE97560 | GEO | 2018/12/07

REPOSITORIES: GEO

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Project description:Kurozu is a traditional Japanese rice vinegar. During fermentation and aging of the Kurozu liquid in an earthenware jar over 1 year, solid residue called Kurozu Moromi is produced. In the present study, we evaluated whether concentrated Kurozu or Kurozu Moromi could ameliorate cognitive dysfunction in the senescence accelerated P8 mouse. Senescence accelerated P8 mice were fed 0.25% (w/w) concentrated Kurozu or 0.5% (w/w) Kurozu Moromi for 4 or 25 weeks. Kurozu suppressed cognitive dysfunction and amyloid accumulation in the brain, while Kurozu Moromi showed a tendency to ameliorate cognitive dysfunction, but the effect was not significant. We hypothesize that concentrated Kurozu has an antioxidant effect, however, the level of lipid peroxidation in the brain did not differ in senescence accelerated P8 mice. DNA microarray analysis indicated that concentrated Kurozu increased HSPA1A mRNA expression, a protein that prevents protein misfolding and aggregation. The increase in HSPA1A expression by Kurozu was confirmed using quantitative real-time PCR and immunoblotting methods. Therefore, the suppression of amyloid accumulation by concentrated Kurozu may be associated with HSPA1A induction. However, concentrated Kurozu could not increase HSPA1A expression in mouse primary neurons, suggesting it may not directly affect neurons. Ten-times concentrated Kurozu (CK) was made from Kurozu liquid (Sakamoto Kurozu, Fukuyama, Kagoshima, Japan) by repeated vacuum distillation. The CK diet included 0.25% (w/w) CK in CE-2 basic rodent diet (Nihon CLEA, Tokyo, Japan). Senescence resistance (R1) and senescence accelerated P8 (P8) mice were purchased from Japan SLC (Shizuoka, Japan). Mice were housed at 25Â±2Â°C with 55Â±10% humidity on a 12-h light/dark cycle (lighting time 08:00-20:00). All mice were housed in independent cages and had free access to food and water. All procedures were compliant with the guidelines of the Kagoshima University Animal Ethics Committee (A10030). Ten-week old R1 mice (n=16) were fed a control CE2 diet and P8 mice were divided into three groups as follows: control CE2 diet group (n=9), KM diet group (n=9) or CK diet group (n=9). Feeding of the experimental diet started from 12 weeks of age until sacrificed. All mice were sacrificed under anesthesia at 17 weeks old (4 months old). The left side of the hippocampus region was excised from brains of 4 mice selected at random in each group, and then subjected to microarray analysis.

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H3K9ac data from mouse models suggest structural changes in the murine brain epigenome that involve the nuclear lamina

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