BDF1 wild type mice vs F33 (HIV-1 Tat-Tg- mice) - Differential thymic microRNA Expression
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE65006 | GEO | 2015/07/06
SECONDARY ACCESSION(S): PRJNA272709
REPOSITORIES: GEO
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Project description:Thymic microRNA expression profiles of wild type vs Tat-Transgenic mice Wild type vs HIV-1 Tat Transgenic mice - microRNA Expression: 3 Biological Replicates The overall experiment included 3 Chip: 1) Wild -type BDF-1 (Cy3) vs F33-Tat-Tg mice (Cy5); 2) F33-Tat-Tg mice (Cy3) vs Wild -type BDF-1 (Cy5); 3) Wild -type BDF-1 (Cy3) vs F33-Tat-Tg mice (Cy5)
2015-07-06 | E-GEOD-65006 | biostudies-arrayexpress
Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent.
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Project description:Previous studies have demonstrated elevated circulating levels of PANcreatic DERived factor (PANDER) overexpression induced a selective hepatic insulin resistant phenotype in the liver of the PANDER transgenic mouse model. Here we utilized SILAC for "spike-in" as a quantitative mass spectrometry based proteomic workflow to reveal proteomic profile changes between the PANDER transgenic mouse and the wild-type mouse.
2016-09-29 | PXD004171 | Pride
Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent. Human fetal neurons were chosen to examine the impact of HIV-1 Tat protein on gene expression
2012-12-07 | E-GEOD-42423 | biostudies-arrayexpress
Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent. Using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs and mRNAs.
2013-02-12 | E-GEOD-44265 | biostudies-arrayexpress
Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent. Human neurons SH-SY5Y were chosen to examine the impact of HIV-1 Tat protein on gene expression
2013-01-17 | E-GEOD-43534 | biostudies-arrayexpress
Project description:We sequenced the mRNA from a stably transduced Human T-cell line expressing the HIV-1 Tat protein. The inducible Tat expression has been used to understand and compare the cellular molecules and pathways being modulated by the wild type subtype-C Tat versus its single signature amino acid residue variant. Additionaly, the HIV-1 subtype B and C Tat comparitive analysis has also been included in the study to evaluate the gene expression profile as a reponse to subtype specific Tat proteins.
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Project description:HIV-1 Tat can modulate the expression of both HIV and cellular genes. In antigen-presenting cells Tat induces the expression of a subset of interferon-stimulated genes (ISGs) in the absence of interferons (IFNs). We investigated the genome-wide Tat association with cellular promoters in immature dendritic cells (iDC) and in monocyte derived macrophages (MDM). Chromatin immunoprecipitation (ChIP) of Tat together with chromatin profiling by ChIP-on-chip analysis demonstrated that Tat associates with the MAP2K6 and MAP2K3 promoters and mediates its increase, which also affects the induction of some ISGs. comparison of KG-1 cells expressing tTA control vs Tat or mutant TatSF2G48R57A
2013-05-31 | E-GEOD-42191 | biostudies-arrayexpress
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.
2016-05-23 | GSE64158 | GEO
Project description:Our goal was to examine whether the HIV Tat peptide, which is usually secreted from infected cells and has the potential to act in other cell types, alters gene expression in the Central Nervous System, and whether a drug abuse co-morbidity, in the case Methamphetamine, can play a role in further modifying gene expression. In order to address the effects of HIV Tat and Methamphetamine, alone and combined, we used an in vivo mouse model that has been described to mimic several aspects of neuroHIV, including changes in inflammatory markers, and decreased expression of dopamine receptors. These animals are transgenic mice, which upon treatment with with doxycycline for 10 days, express TAT protein under the control of the glial fibrilary associated protein (GFAP) promoter in the brain. They were treated with Meth and Saline for identification of gene expression changes that result from Tat or Methamphetamine alone, or from their interaction. There was an overall suppression of gene expression by Methamphetamine, in Tat- mice. The expression of Tat caused most Meth-induced changes to remain at control levels.
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