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      microRNA expression in the prefrontal cortex of individuals with schizophrenia and schizoaffective disorder

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          Abstract

          Transcriptional profiling reveals a possible association between schizophrenia and altered miRNA expression

          Abstract

          Background

          microRNAs (miRNAs) are small, noncoding RNA molecules that are now thought to regulate the expression of many mRNAs. They have been implicated in the etiology of a variety of complex diseases, including Tourette's syndrome, Fragile × syndrome, and several types of cancer.

          Results

          We hypothesized that schizophrenia might be associated with altered miRNA profiles. To investigate this possibility we compared the expression of 264 human miRNAs from postmortem prefrontal cortex tissue of individuals with schizophrenia ( n = 13) or schizoaffective disorder ( n = 2) to tissue of 21 psychiatrically unaffected individuals using a custom miRNA microarray. Allowing a 5% false discovery rate, we found that 16 miRNAs were differentially expressed in prefrontal cortex of patient subjects, with 15 expressed at lower levels (fold change 0.63 to 0.89) and 1 at a higher level (fold change 1.77) than in the psychiatrically unaffected comparison subjects. The expression levels of 12 selected miRNAs were also determined by quantitative RT-PCR in our lab. For the eight miRNAs distinguished by being expressed at lower microarray levels in schizophrenia samples versus comparison samples, seven were also expressed at lower levels with quantitative RT-PCR.

          Conclusion

          This study is the first to find altered miRNA profiles in postmortem prefrontal cortex from schizophrenia patients.

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          Most cited references 37

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          In silico prediction of protein-protein interactions in human macrophages

          Background: Protein-protein interaction (PPI) network analyses are highly valuable in deciphering and understanding the intricate organisation of cellular functions. Nevertheless, the majority of available protein-protein interaction networks are context-less, i.e. without any reference to the spatial, temporal or physiological conditions in which the interactions may occur. In this work, we are proposing a protocol to infer the most likely protein-protein interaction (PPI) network in human macrophages. Results: We integrated the PPI dataset from the Agile Protein Interaction DataAnalyzer (APID) with different meta-data to infer a contextualized macrophage-specific interactome using a combination of statistical methods. The obtained interactome is enriched in experimentally verified interactions and in proteins involved in macrophage-related biological processes (i.e. immune response activation, regulation of apoptosis). As a case study, we used the contextualized interactome to highlight the cellular processes induced upon Mycobacterium tuberculosis infection. Conclusion: Our work confirms that contextualizing interactomes improves the biological significance of bioinformatic analyses. More specifically, studying such inferred network rather than focusing at the gene expression level only, is informative on the processes involved in the host response. Indeed, important immune features such as apoptosis are solely highlighted when the spotlight is on the protein interaction level.
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            A brain-specific microRNA regulates dendritic spine development.

            MicroRNAs are small, non-coding RNAs that control the translation of target messenger RNAs, thereby regulating critical aspects of plant and animal development. In the mammalian nervous system, the spatiotemporal control of mRNA translation has an important role in synaptic development and plasticity. Although a number of microRNAs have been isolated from the mammalian brain, neither the specific microRNAs that regulate synapse function nor their target mRNAs have been identified. Here we show that a brain-specific microRNA, miR-134, is localized to the synapto-dendritic compartment of rat hippocampal neurons and negatively regulates the size of dendritic spines--postsynaptic sites of excitatory synaptic transmission. This effect is mediated by miR-134 inhibition of the translation of an mRNA encoding a protein kinase, Limk1, that controls spine development. Exposure of neurons to extracellular stimuli such as brain-derived neurotrophic factor relieves miR-134 inhibition of Limk1 translation and in this way may contribute to synaptic development, maturation and/or plasticity.
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              MicroRNA Targets in Drosophila

              Additional data files Additional data file 1, 2, 3 and 4. Supplementary Material Additional data file 1 Additional data file 1 Click here for additional data file Additional data file 2 Additional data file 2 Click here for additional data file Additional data file 3 Additional data file 3 Click here for additional data file Additional data file 4 Additional data file 4 Click here for additional data file
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                Author and article information

                Journal
                Genome Biol
                Genome Biology
                BioMed Central (London )
                1465-6906
                1465-6914
                2007
                27 February 2007
                : 8
                : 2
                : R27
                Affiliations
                [1 ]Department of Psychiatry, University of North Carolina at Chapel Hill, CB 7160, Chapel Hill, NC 27599, USA
                [2 ]School of Pharmacy, University of North Carolina at Chapel Hill, CB 7360, Chapel Hill, NC 27599, USA
                [3 ]Renaissance Computing Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
                [4 ]Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, CB 7090, Chapel Hill, NC 27599, USA
                [5 ]Constella Group, LLC, Meridian Parkway, Durham, NC 27713, USA
                [6 ]Department of Molecular Biology, University of North Carolina at Chapel Hill, CB 7104, Chapel Hill, NC 27599, USA
                Article
                gb-2007-8-2-r27
                10.1186/gb-2007-8-2-r27
                1852419
                17326821
                Copyright © 2007 Perkins et al.; licensee BioMed Central Ltd.

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research

                Genetics

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