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HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments [Bisulfite-seq]

ABSTRACT: To investigate whole genomic DNA methylation changes after cocaine/saline treatment in iTat mice, we isolated genomic DNA from 24 hippocampus hemispheres of mice and performed whole genomic bisulfite sequencing (WGBS).

ORGANISM(S): Mus musculus

PROVIDER: GSE200254 | GEO | 2022/04/07

REPOSITORIES: GEO

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HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments [RNA-seq]

Project description:To investigate RNA expression changes after cocaine/saline treatment in iTat mice, we isolated RNA from the other 24 corresponding hippocampus hemispheres of the same mice (used for WGBS) and performed bulky RNA sequencing. We then did the gene expression analysis and correlated the genen expression data with WGBS data.

2022-04-07 | GSE200189 | GEO

HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-04-07 | GSE200255 | GEO

HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments

Project description:HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments

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HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments [RNA-seq]

Project description:HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments [RNA-seq]

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HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments [Bisulfite-seq]

Project description:HIV Tat and cocaine interactively alter genome-wide DNA methylation and gene expression and exacerbate learning and memory impairments [Bisulfite-seq]

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Genomic sensitization in response to G9a repression following repeated cocaine exposure

Project description:Cocaine-induced alterations in gene expression cause changes in neuronal morphology and behavior that may underlie cocaine addiction. We identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity. Repeated cocaine administration reduced global levels of H3K9 dimethylation in the nucleus accumbens. This reduction in histone methylation was mediated through the repression of G9a in this brain region. To identify whether changes in H3K9me2 correlated with genome-wide alterations in gene expression in the NAc, we employed microarray analyses to examine gene expression profiles induced by a challenge dose of cocaine in animals with or without a history of prior cocaine exposure. Animals that had received repeated cocaine displayed dramatically increased gene expression 1 hour after a cocaine challenge in comparison to acutely treated animals. This increased gene expression still occurred in response to a cocaine challenge given after 1 week of withdrawal from repeated cocaine. These data suggest that repeated, but not acute, cocaine exposure results in persistent sensitized genomic responses to a cocaine challenge, indicating that sensitized behavioral responses to repeated cocaine are likely the result of G9a-dependent alterations in global transcriptional responses to cocaine.

2009-10-28 | GSE18751 | GEO

Cocaine and Environmental Enrichment Proteomics Study of Rat Nucleus Accumbens

Project description:Prior research demonstrated that environmental enrichment creates individual differences in behavior leading to a protective addiction phenotype in rats. Understanding the mechanisms underlying this phenotype will guide selection of targets for much-needed novel pharmacotherapeutics. The current study investigates basal differences in proteome expression in the nucleus accumbens of enriched and isolated rats and the proteomic response to cocaine self-administration using a liquid chromatography mass spectrometry (LCMS) technique to quantify 1917 proteins. Results of complementary Ingenuity Pathways Analyses (IPA) and gene set enrichment analyses (GSEA) demonstrate that cocaine increases vesicular transporters for dopamine and glutamate, as well as increasing proteins in the RhoA pathway. Further, cocaine regulates proteins related to ERK, CREB and AKT signaling. Environmental enrichment altered expression of a large number of proteins with diverse functions, including mood disorders, energy production, ubiquitination, splicing, transport, kinases and neurodegenerative diseases. Most of the biological functions and pathways listed above were also identified in the Cocaine X Enrichment interaction analysis, providing clear evidence that enriched and isolated rats respond quite differently to cocaine exposure. The overall impression of the current results is that enriched saline-administering rats have a unique proteomic complement compared to enriched cocaine-administering rats as well as saline and cocaine-taking isolated rats. These results identify possible mechanisms of the protective phenotype and provide fertile soil for developing novel pharmacotherapeutics.

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Inhibition of the Dead Box RNA Helicase 3 prevents HIV-1 Tat and cocaine-induced neurotoxicity by targeting microglia activation

Project description:We have investigated the protective effect of DDX3 inhibitor RK33 on toxic damage done by combined TAT and cocaine.

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ChIP-Seq reveals regulation of the heterochromatic mark, H3K9me3, in NAc following repeated cocaine administration

Project description:Repeated administration of the psychostimulant cocaine has been shown to produce persistent alterations in genome-wide transcriptional regulatory networks, chromatin remodeling activity and, ultimately, gene expression profiles in the brain’s reward circuitry. Virtually all previous investigations have centered on drug-mediated effects occurring throughout active euchromatic regions of the genome, such that very little is known concerning the impact of cocaine exposure on the regulation and maintenance of heterochromatin in adult brain. Here, we report that cocaine administration dramatically and dynamically alters heterochromatic histone H3 lysine 9 trimethylation (H3K9me3) in the nucleus accumbens (NAc), a key brain reward region. Furthermore, we demonstrate that repeated cocaine exposure induces persistent decreases in heterochromatization in this brain region, suggesting a potential role for heterochromatic regulation in the long-term actions of cocaine. To identify precise genomic loci affected by these alterations, chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-Seq) was performed on NAc. ChIP-Seq analyses confirmed the existence of the H3K9me3 mark mainly within inter-genic regions of the genome and identified specific patterns of cocaine-induced H3K9me3 regulation at repetitive genomic sequences. Cocaine-mediated decreases in H3K9me3 enrichment at specific genomic repeats (e.g., LI repeats) were further confirmed by the increased expression of LINE-1 and IAP retrotransposons in NAc. Such increases likely reflect global patterns of genomic de-stabilization in this brain region following repeated cocaine administration and open the door for future investigations into the epigenetic and genetic basis of drug addiction.

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Cocaine perturbs mitovesicle biology in the brain

Project description:Cocaine is one of the most abused psychostimulants in the United States. In addition to its established roles in the regulation of dopaminergic circuitries, cocaine has a broader mechanism of action, including global alterations in brain metabolism and mitochondrial homeostasis. Our group recently identified a subpopulation of non-microvesicular, non-exosomal extracellular vesicles of mitochondrial origin, mitovesicles (mtVs), and provided a method to isolate mtVs from brain parenchyma. Given their origin, we hypothesized that mtVs could be affected by mitochondrial abnormalities induced by chronic cocaine exposure. Therefore, we analyzed mtVs from hemibrains of 3-month-old mice that received for two weeks intraperitoneal injections of cocaine or saline as control. MtVs from the brain extracellular space of cocaine-intoxicated mice were enlarged and more numerous when compared to controls. Moreover, cocaine stimulated higher intracellular mitochondrial fission and higher levels of upstream (but not downstream) mitophagy pathways, suggesting increased mitochondrial fragmentation and a block in mitophagy flux. Lastly, cocaine impaired brain mtV cargo loading as revealed by Mass Spec analysis, causing an alteration in mtV ATP production capacity. These data suggest that mtVs are a previously unidentified player in the biology of cocaine addiction and that target therapies to fine tune brain mtV functionality may be beneficial to mitigate chronic cocaine pathology.

2022-04-27 | MSV000089323 | MassIVE

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