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Neuropsychiatric and clinical correlates to miRNA expression in the frontal cortex of HIV-infected individuals

ABSTRACT: Objective: To elucidate molecular mechanisms of neurocognitive dysfunction in long-term HIV-infected individuals by assessing the microRNA (miR) profile and determining clinical and neurocognitive correlates to miR expression. Design: Analysis of miR profile in frontal cortex of retrospectively-identified autopsy cases of longitudinally-followed subjects with HIV-infection and age/sex-matched controls. HIV-subjects had semi-annual neuropsychiatric and clinical testing, at autopsy, tissue was archived. Methods: MiR repertoires were profiled from frontal cortices. Analysis of variance (ANOVA) and Tukey Honestly Sigificant Difference (HSD) tests with Benjamini-Hochberg correction for multiple comparisons were used to compare expression among the three groups. Pairwise correlations were used to identify neuropsychiatric variable that correlatee with expression of miRs. Results: MiRs were significantly different by HIV-status: miR-103, miR-125a, miR-380, miR-422a, miR-515, miR-520b, miR0618, miR-886, and miR-9. Many miRs correlated with neuropsychiatric outcomes like Learning, Memory, Executive, Verbal, and Motor deficit scores. Conclusions: MiRs are clearly dysregulated in the frontal cortex of HIV-positive individuals. Only a few miRs were significantly dysregulated in only the methamphetamine group. Our study identifies miRs that form rational targets for further inquiry on biochemical mechanisms of HIV-related neurocognitive deficits. Learning deficit score correlates with expression of more miRs than other parameters.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41952 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA179440

REPOSITORIES: GEO

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Neuropsychiatric and clinical correlates to miRNA expression in the frontal cortex of HIV-infected individuals

Project description:Objective: To elucidate molecular mechanisms of neurocognitive dysfunction in long-term HIV-infected individuals by assessing the microRNA (miR) profile and determining clinical and neurocognitive correlates to miR expression. Design: Analysis of miR profile in frontal cortex of retrospectively-identified autopsy cases of longitudinally-followed subjects with HIV-infection and age/sex-matched controls. HIV-subjects had semi-annual neuropsychiatric and clinical testing, at autopsy, tissue was archived. Methods: MiR repertoires were profiled from frontal cortices. Analysis of variance (ANOVA) and Tukey Honestly Sigificant Difference (HSD) tests with Benjamini-Hochberg correction for multiple comparisons were used to compare expression among the three groups. Pairwise correlations were used to identify neuropsychiatric variable that correlatee with expression of miRs. Results: MiRs were significantly different by HIV-status: miR-103, miR-125a, miR-380, miR-422a, miR-515, miR-520b, miR0618, miR-886, and miR-9. Many miRs correlated with neuropsychiatric outcomes like Learning, Memory, Executive, Verbal, and Motor deficit scores. Conclusions: MiRs are clearly dysregulated in the frontal cortex of HIV-positive individuals. Only a few miRs were significantly dysregulated in only the methamphetamine group. Our study identifies miRs that form rational targets for further inquiry on biochemical mechanisms of HIV-related neurocognitive deficits. Learning deficit score correlates with expression of more miRs than other parameters. A total of 11 HIV positive individuals were analyzed, 5 of which had a past history of methamphetamine ABUSE, and 5 age-matched HIV-negative normal Controls. Technical duplicates are included. Included are clinical and neuropsychiatric data from most recent visit before time of death. This is a retrospective autopsy study of longitudinally-followed subjects on miRNA levels in the frontal cortex.

2013-01-01 | E-GEOD-41952 | biostudies-arrayexpress

Gene Expression in Frontal Cortex in Major Depression and HIV

Project description:Major depressive disorder (MDD) is a clinically defined entity with little understanding as to the underlying pathological substrate. Biologically, MDD is characterized by disruption of neurotransmitters, especially serotonin and noradrenaline, which are the main targets of antidepressants. We previously demonstrated significant reduction of glial cell number in the cingulate and dorsolateral prefrontal cortical regions. Unfortunately, individuals living with HIV still have very high rates of MDD, despite the fact that mortality rates have fallen sharply with effective antiretroviral treatment. It is possible that in this treatment era, living with chronic HIV infection may result in long-term neuropathological changes that predispose to MDD. For example, it is known that HIV is associated with a range of inflammatory pathologies, neuronal loss, and dendrite-synaptic damage. In HIV, these neurodegenerative changes have been linked to neurocognitive impairments, however it is also possible that these changes potentiate MDD. In the current study, we sought to determine whether there are changes in gene expression in the MDD brain in the frontal cortex in HIV-context. We identify a large number of genes dysregulated at p<0.05 significance. Retrospective gene expression analysis of autopsy brain tissue. Four HIV/MDD subjects are identified and age-matched HIV patients without neuropsychiatric conditions are compared as controls.

2010-02-01 | E-GEOD-17440 | biostudies-arrayexpress

Host response and dysfunction in the CNS during chronic simian immunodeficiency virus infection [human study]

Project description:Finding the differences in gene expression in three regions of the brai, basal ganglia, white matter, and frontal cortex, in normal, HIV infected, HIV inefected with neurocognitive impairment, and HIV infected with both neurocognitive impairment and encephalitis patients. We used microarrays to identify differentially expressed genes in normal, HIV infected, HIV inefected with neurocognitive impairment, and HIV infected with both neurocognitive impairment and encephalitis patients. Samples from three different brain regions from normal, HIV infected, HIV infected with neurocognitive impairment (HAD: HIV-associated dementia), and HIV infected with both neurocognitive impairment and encephalitis (HIVE: HIV encephalitis) patients were collected for RNA isolation and supsequent Affymetrix microarray analysis. We sought to obtain gene expression levels in different brain regions to find implication of HIV and the neurological impairment and inflammation associated with HIV infection.

2012-07-31 | E-GEOD-35864 | biostudies-arrayexpress

The National NeuroAIDS Tissue Consortium Brain Gene Array: Two types of HIV-associated neurocognitive impairment

Project description:Finding the differences in gene expression in three regions of the brain, basal ganglia, white matter, and frontal cortex, in normal, HIV infected, HIV infected with neurocognitive impairment, and HIV infected with both neurocognitive impairment and encephalitis patients.

2012-08-01 | GSE35864 | GEO

Homo sapiens

Project description:Neuropsychiatric and clinical correlates to miRNA expression in the frontal cortex of HIV-infected individuals

| PRJNA179440 | ENA

Transcriptomic analysis of brian tissues identifies a role for CCAAT enhancer binding protein β in HIV- associated neurocognitive disorder

Project description:In this study, using 33 postmortem frontal cortex (FC) tissues, neuropathological, molecular, and biochemical analyses were used to determine cellular localization and validate expression levels of the prolific transcription factor (TF), CCAAT enhancer binding protein (C/EBP) β, in brain tissues from HIV+ cognitively normal and HAND cases. RNA sequencing (seq) and transcriptomic analyses were performed on FC tissues including 24 specimens from well-characterized people with HIV that had undergone neurocognitive assessments. In vitro models for brain cells were used to investigate the role of C/EBPβ in mediating gene expression.

2020-06-16 | GSE152461 | GEO

ena-DATASET-VUMC-CCA-23-10-2015-09:58:10:052-218 - samples

Project description:MicroRNAs (miRs) have been recognized as promising biomarkers. It is unknown to what extent tumor-derived miRs are differentially expressed between primary colorectal cancers (pCRCs) and metastatic lesions, and to what extent the expression profiles of tumor tissue differ from the surrounding normal tissue. Next-generation sequencing (NGS) of 220 fresh-frozen samples, including paired primary and metastatic tumor tissue and non-tumorous tissue from 38 patients, revealed expression of 2245 known unique mature miRs and 515 novel candidate miRs. Unsupervised clustering of miR expression profiles of pCRC tissue with paired metastases did not separate the two entities, whereas unsupervised clustering of miR expression profiles of pCRC with normal colorectal mucosa demonstrated complete separation of the tumor samples from their paired normal mucosa. Two hundred and twenty-two miRs differentiated both pCRC and metastases from normal tissue samples (false discovery rate (FDR) <0.05). The highest expressed tumor-specific miRs were miR-21 and miR-92a, both previously described to be involved in CRC with potential as circulating biomarker for early detection. Only eight miRs, 0.5% of the analysed miR transcriptome, were differentially expressed between pCRC and the corresponding metastases (FDR <0.1), consisting of five known miRs (miR-320b, miR-320d, miR-3117, miR-1246 and miR-663b) and three novel candidate miRs (chr 1-2552-5p, chr 8-20656-5p and chr 10-25333-3p). These results indicate that previously unrecognized candidate miRs expressed in advanced CRC were identified using NGS. In addition, miR expression profiles of pCRC and metastatic lesions are highly comparable and may be of similar predictive value for prognosis or response to treatment in patients with advanced CRC.

| EGAD00001001644 | EGA

MiR expression profiles of paired primary colorectal cancerand metastases by next-generation sequencing

Project description:MicroRNAs (miRs) have been recognized as promising biomarkers. It is unknown to what extent tumor-derived miRs are differentially expressed between primary colorectal cancers (pCRCs) and metastatic lesions, and to what extent the expression profiles of tumor tissue differ from the surrounding normal tissue. Next-generation sequencing (NGS) of 220 fresh-frozen samples, including paired primary and metastatic tumor tissue and non-tumorous tissue from 38 patients, revealed expression of 2245 known unique mature miRs and 515 novel candidate miRs. Unsupervised clustering of miR expression profiles of pCRC tissue with paired metastases did not separate the two entities, whereas unsupervised clustering of miR expression profiles of pCRC with normal colorectal mucosa demonstrated complete separation of the tumor samples from their paired normal mucosa. Two hundred and twenty-two miRs differentiated both pCRC and metastases from normal tissue samples (false discovery rate (FDR) o0.05). The highest expressed tumor-specific miRs were miR-21 and miR-92a, both previously described to be involved in CRC with potential as circulating biomarker for early detection. Only eight miRs, 0.5% of the analysed miR transcriptome, were differentially expressed between pCRC and the corresponding metastases (FDR o0.1), consisting of five known miRs (miR-320b, miR-320d, miR-3117, miR-1246 and miR-663b) and three novel candidate miRs (chr 1-2552-5p, chr 8-20656-5p and chr 10-25333-3p). These results indicate that previously unrecognized candidate miRs expressed in advanced CRC were identified using NGS. In addition, miR expression profiles of pCRC and metastatic lesions are highly comparable and may be of similar predictive value for prognosis or response to treatment in patients with advanced CRC

| EGAS00001001127 | EGA

Unique Circulating MicroRNA profiles in HIV Infection

Project description:We aimed to determine the association between extracellular miRs and HIV infection, and have demonstrated unique expression profile of 29 miRs in HIV+ subjects and 34 miRs in elite controllers as compared to HIV- subjects. Elite HIV+ subjects are those who are HIV+, not on antiretroviral therapy, and with HIV viral load <200 copies/mL.

2018-02-14 | GSE110552 | GEO

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders

Project description:Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Human fetal neurons were chosen to examine the impact of HIV-1 Vpr protein on gene expression

2012-12-07 | E-GEOD-42424 | biostudies-arrayexpress

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