Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA229484 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Effects of GDM involves alterations in gene specific DNA methylation
| PRJNA274993 | ENA
Project description:Antipsychotic drugs are commonly used to treat psychosis, mood disorders, and anxiety. While there is indirect evidence that some component of the antipsychotic effect of these drugs may involve modulation of dopamine transmission, their mechanism of action is poorly understood. We hypothesized that antipsychotic drugs mediate their effects via epigenetic modulation. Here we tested the effect of an antipsychotic, olanzapine, on the methylation status of genes following chronic treatment. These effects have been revealed through significantly increased (p<0.01) DNA methylation of genes involved in dopaminergic and non-dopaminergic pathways including the glutamatergic, GABAergic, cholinergic, neuregulin and ErbB signaling pathways. The affected genes included GLS in hippocampus, NR1 in cerebellum and GLUD1 and NR2B in liver. Further, from a set of genes in the 22q11.2 micro-deletions that has been previously implicated in psychosis, 22 genes showed increased methylation following olanzapine treatment. Ingenuity Pathway Analysis (IPA) revealed that chronic olanzapine treatment significantly affected several important pathways such as CREB and CDK5 signaling (p=1.4E-05). Also, DNA replication, recombination and repair, cellular movement and cell cycle have been identified as the top networks affected by olanzapine. The results suggest that these downstream effects, aside from D2 blockade, may play a critical role in the biological actions of antipsychotics. These include altered expressions of relevant genes involved in GABAergic, glutamatergic, cholinergic, neuregulin and ErbB signaling pathways. Epigenetic mechanisms involving changes in DNA methylation could, therefore, explain the delay and individualized non-specificity of biological effects of olanzapine. The results also suggest that DNA methylation may play a role in the process of therapeutic efficacy of olanzapine by altering the transcriptome via tissue-specific methylation of genes involved in schizophrenia signaling pathways. comparison of olanzapine treated rats vs. control rats for genome-wide DNA methylation changes
2013-11-22 | E-GEOD-52615 | biostudies-arrayexpress
Project description:Antipsychotic drugs are commonly used to treat psychosis, mood disorders, and anxiety. While there is indirect evidence that some component of the antipsychotic effect of these drugs may involve modulation of dopamine transmission, their mechanism of action is poorly understood. We hypothesized that antipsychotic drugs mediate their effects via epigenetic modulation. Here we tested the effect of an antipsychotic, olanzapine, on the methylation status of genes following chronic treatment. These effects have been revealed through significantly increased (p<0.01) DNA methylation of genes involved in dopaminergic and non-dopaminergic pathways including the glutamatergic, GABAergic, cholinergic, neuregulin and ErbB signaling pathways. The affected genes included GLS in hippocampus, NR1 in cerebellum and GLUD1 and NR2B in liver. Further, from a set of genes in the 22q11.2 micro-deletions that has been previously implicated in psychosis, 22 genes showed increased methylation following olanzapine treatment. Ingenuity Pathway Analysis (IPA) revealed that chronic olanzapine treatment significantly affected several important pathways such as CREB and CDK5 signaling (p=1.4E-05). Also, DNA replication, recombination and repair, cellular movement and cell cycle have been identified as the top networks affected by olanzapine. The results suggest that these downstream effects, aside from D2 blockade, may play a critical role in the biological actions of antipsychotics. These include altered expressions of relevant genes involved in GABAergic, glutamatergic, cholinergic, neuregulin and ErbB signaling pathways. Epigenetic mechanisms involving changes in DNA methylation could, therefore, explain the delay and individualized non-specificity of biological effects of olanzapine. The results also suggest that DNA methylation may play a role in the process of therapeutic efficacy of olanzapine by altering the transcriptome via tissue-specific methylation of genes involved in schizophrenia signaling pathways.
2013-11-22 | GSE52615 | GEO
Project description:Antipsychotic drugs are classified as typical and atypical based on extrapyramidal effects. However, since the frontal cortex is one of the most important regions for antipsychotic actions, this study attempted to classify antipsychotic drugs based on gene expression in the frontal cortex. Chlorpromazine and thioridazine were selected as typical antipsychotics, and olanzapine and quetiapine as atypical antipsychotics. Since these drugs have similar chemical structures, the effect of the basic structure on gene expression can be eliminated. Cluster analysis of microarray experiments showed thioridazine and olanzapine constituted a robust cluster. K-means clustering separated 4-drug-administered mice into chlorpromazine-quetiapine and thioridazine-olanzapine groups. This classification scheme is different from that which is based on criteria currently used to group the typical and atypical drugs and suggests that antipsychotic drugs can be further separated into multiple groups. Keywords: repeat sample
2004-09-24 | GSE1501 | GEO
Project description:Male Sprague-Dawley albino rats (Charles River) initially weighting approximately 200 grams were randomly assigned to one of the following: 1) olanzapine (2 mg/kg/day, I.P.) (N=20) or 2) Saline (N=20) and administered olanzapine or saline for 21 days. Frontal cortex (N=4/group) was dissected and homogenized for microarray, QPCR and western blotting following previous methods (Fatemi et al. 2003; Brooks et al. 2003). RNA isolation, cDNA preparation, microarray hybridization and QPCR followed previous methods (Brooks et al. 2003).
2007-11-03 | E-GEOD-2547 | biostudies-arrayexpress
Project description:Tissue-specific dysregulation of DNA methylation in aging
| PRJNA119017 | ENA
Project description:Epigenetic histone modificationshave been found to be associated with the development of metabolic disorders.However,the potential contribution of these modifications to metabolic disturbances induced by chronic treatment with second-generation antipsychotic drugs (SGAs) remains unclear. This study presents chromatin immunoprecipitation (ChIP) data on H3K4me methylation in hepatic tissue of rats treated with olanzapine or clozapine for 9 weeks.This dataset provides a comprehensive view of the effects of SGAs on H3K4me methylation in an animal model, offering new insights into the epigenetic mechanisms underlying SGAs-induced metabolic side effects.
2025-01-29 | GSE288060 | GEO
Project description:Analysis of gene expression in the striatum, the liver, the pancreas, and the visceral adipose tissue of mice treated for 28 days with a daily dose of an atypical antipsychotic: risperidone (1 mg/kg) or olanzapine (3.5 mg/kg). Results provide new insights into the molecular mechanisms underlying antipschotic effects, particularly in tissues relevant for antipsychotic-induced metabolic dysregulation. Antipsychotics are associated with weight gain and other metabolic abnormalities such as hyperglycemia, dyslipidemia and metabolic syndrome. We used microarrays to uncover the underlying molecular mechanisms and identify the key genes involved in AP-induced metabolic effects.
2021-09-08 | GSE180473 | GEO
Project description:In this study, a comprehensive evaluation model for studying the cardiac toxicity of antipsychotic drugs was established by using iPSC-CMs. Six antipsychotic drugs, including aripiprazole, risperidone, quetiapine, haloperidol, clozapine, and olanzapine, all induced concentration-dependent QT prolongation in iPSC-CMs upon acute administration, and high concentrations of these drugs caused disorganized sarcomere arrangement in iPSC-CMs.
2024-01-01 | GSE248368 | GEO