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

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

PROVIDER: PRJNA823748 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18637700.fastq.gz	Fastqsanger.gz
	SRR18650629_1.fastq.gz	Fastqsanger.gz
	SRR18650629_2.fastq.gz	Fastqsanger.gz
	SRR18650630_1.fastq.gz	Fastqsanger.gz
	SRR18650630_2.fastq.gz	Fastqsanger.gz

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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]

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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]

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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.

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

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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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Methamphetamine and HIV-Tat Alter Murine Cardiac DNA Methylation and Gene Expression [Methylation]

Project description:This study addresses the individual and combined effects of HIV-1 and methamphetamine (N-methyl-1-phenylpropan-2-amine, METH) on cardiac dysfunction in a transgenic mouse model of HIV/AIDS. METH is abused epidemically and is frequently associated with acquisition of HIV-1 infection or AIDS. We employed microarrays to identify mRNA differences in cardiac left ventricle (LV) gene expression following METH administration (10d, 3mg/kg/d, subcutaneously) in C57Bl/6 wild-type littermates (WT) and Tat-expressing transgenic (TG) mice. Arrays identified 880 differentially expressed genes (expression fold change>1.5, p<0.05) following METH exposure, Tat expression, or both. Using pathway enrichment analysis, mRNAs encoding polypeptides for calcium signaling and contractility were altered in the LV samples. Correlative DNA methylation analysis revealed significant LV DNA methylation changes following METH exposure and Tat expression. By combining these data sets, 38 gene promoters (27 related to METH, 11 related to Tat) exhibited differences by both methods of analysis. Among those, only the promoter for CACNA1C that encodes L-type calcium channel Cav1.2 displayed DNA methylation changes concordant with its gene expression change. Quantitative PCR verified that Cav1.2 LV mRNA abundance doubled following METH. Correlative immunoblots specific for Cav1.2 revealed a 3.5-fold increase in protein abundance in METH LVs. Data implicate Cav1.2 in calcium dysregulation and hypercontractility in the murine LV exposed to METH. They suggest a pathogenetic role for METH exposure to promote LV dysfunction that outweighs Tat-induced effects. This study addresses how HIV-1 and methamphetamine comorbidities affect cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation.

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Single neuron analysis of aging associated changes in learning reveals escalating impairments in transcriptional plasticity

Project description:Molecular mechanisms underlying aging associated impairments in learning and long-term memory storage are poorly understood. Here we leveraged an identified motor neuron L7, mediating long-term sensitization of siphon-withdrawal reflex, a form of non-associative learning in sea slug Aplysia, to assess the impact of aging on transcriptional changes during learning. RNAseq analysis of single L7 motor neuron isolated following short-term or long-term sensitization training from 8,10 and 12 months old Aplysia corresponding to mature, late mature and senescent stages have identified progressive impairments in transcriptional plasticity during aging. Specifically, we uncover modulation of the expression of multiple lncRNAs, and mRNAs encoding transcription factors, regulators of translation, RNA methylation, and cytoskeletal rearrangements during learning and their deficits during aging. Our comparative gene expression analysis also revealed the recruitment of specific transcriptional changes in two other neurons, a motor neuron L11 and giant cholinergic neuron R2 whose roles in long-term sensitization were previously not known. Taken together, our analyses establish cell type specific escalating impairments in the expression of learning and LTM relevant components of transcriptomes during aging.

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