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      Alteration of the microRNA network during the progression of Alzheimer's disease

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          Abstract

          An overview of miRNAs altered in Alzheimer's disease (AD) was established by profiling the hippocampus of a cohort of 41 late-onset AD (LOAD) patients and 23 controls, showing deregulation of 35 miRNAs. Profiling of miRNAs in the prefrontal cortex of a second independent cohort of 49 patients grouped by Braak stages revealed 41 deregulated miRNAs. We focused on miR-132-3p which is strongly altered in both brain areas. Downregulation of this miRNA occurs already at Braak stages III and IV, before loss of neuron-specific miRNAs. Next-generation sequencing confirmed a strong decrease of miR-132-3p and of three family-related miRNAs encoded by the same miRNA cluster on chromosome 17. Deregulation of miR-132-3p in AD brain appears to occur mainly in neurons displaying Tau hyper-phosphorylation. We provide evidence that miR-132-3p may contribute to disease progression through aberrant regulation of mRNA targets in the Tau network. The transcription factor (TF) FOXO1a appears to be a key target of miR-132-3p in this pathway.

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          MicroRNA profiling: approaches and considerations.

          Colin C Pritchard, Heather H Cheng, Muneesh Tewari (2012)
          MicroRNAs (miRNAs) are small RNAs that post-transcriptionally regulate the expression of thousands of genes in a broad range of organisms in both normal physiological contexts and in disease contexts. miRNA expression profiling is gaining popularity because miRNAs, as key regulators in gene expression networks, can influence many biological processes and also show promise as biomarkers for disease. Technological advances have spawned a multitude of platforms for miRNA profiling, and an understanding of the strengths and pitfalls of different approaches can aid in their effective use. Here, we review the major considerations for carrying out and interpreting results of miRNA-profiling studies.
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            A cAMP-response element binding protein-induced microRNA regulates neuronal morphogenesis.

            Ngan H. Vo, Matthew E. Klein, Olga Varlamova … (2005)
            MicroRNAs (miRNAs) regulate cellular fate by controlling the stability or translation of mRNA transcripts. Although the spatial and temporal patterning of miRNA expression is tightly controlled, little is known about signals that induce their expression nor mechanisms of their transcriptional regulation. Furthermore, few miRNA targets have been validated experimentally. The miRNA, miR132, was identified through a genome-wide screen as a target of the transcription factor, cAMP-response element binding protein (CREB). miR132 is enriched in neurons and, like many neuronal CREB targets, is highly induced by neurotrophins. Expression of miR132 in cortical neurons induced neurite outgrowth. Conversely, inhibition of miR132 function attenuated neuronal outgrowth. We provide evidence that miR132 regulates neuronal morphogenesis by decreasing levels of the GTPase-activating protein, p250GAP. These data reveal that a CREB-regulated miRNA regulates neuronal morphogenesis by responding to extrinsic trophic cues.
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              MicroRNA profiling of multiple sclerosis lesions identifies modulators of the regulatory protein CD47.

              Andreas Junker, Markus Krumbholz, Sylvia Eisele … (2009)
              We established microRNA profiles from active and inactive multiple sclerosis lesions. Using laser capture microdissection from multiple sclerosis lesions to pool single cells and in vitro cultures, we assigned differentially expressed microRNA to specific cell types. Astrocytes contained all 10 microRNA that were most strongly upregulated in active multiple sclerosis lesions, including microRNA-155, which is known to modulate immune responses in different ways but so far had not been assigned to central nervous system resident cells. MicroRNA-155 was expressed in human astrocytes in situ, and further induced with cytokines in human astrocytes in vitro. This was confirmed with astrocyte cultures from microRNA-155-|-lacZ mice. We matched microRNA upregulated in phagocytically active multiple sclerosis lesions with downregulated protein coding transcripts. This converged on CD47, which functions as a 'don't eat me' signal inhibiting macrophage activity. Three microRNA upregulated in active multiple sclerosis lesions (microRNA-34a, microRNA-155 and microRNA-326) targeted the 3'-untranslated region of CD47 in reporter assays, with microRNA-155 even at two distinct sites. Our findings suggest that microRNA dysregulated in multiple sclerosis lesions reduce CD47 in brain resident cells, releasing macrophages from inhibitory control, thereby promoting phagocytosis of myelin. This mechanism may have broad implications for microRNA-regulated macrophage activation in inflammatory diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): EMBO Mol Med
                Journal ID (iso-abbrev): EMBO Mol Med
                Journal ID (publisher-id): emmm
                Title: EMBO Molecular Medicine
                Publisher: Blackwell Publishing Ltd
                ISSN (Print): 1757-4676
                ISSN (Electronic): 1757-4684
                Publication date (Print): October 2013
                Publication date (Electronic): 09 September 2013
                Volume: 5
                Issue: 10
                Pages: 1613-1634
                Affiliations
                [1 ]VIB Center for the Biology of Disease Leuven, Belgium
                [2 ]Center for Human Genetics, Leuven Institute for Neurodegenerative Disorders (LIND) University Hospitals Leuven, and University of Leuven O&N4, Herestraat, Leuven, Belgium
                [3 ]Neurogeneration Group, Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences Amsterdam, The Netherlands
                [4 ]Laboratory of Computational Biology, Center for Human Genetics and University of Leuven O&N4, Herestraat, Leuven, Belgium
                [5 ]Department of Biological Chemistry, the Silberman Institute of Life Sciences, and the Edmond and Lily Safra Center of Brain Science Interdisciplinary Center for Neural Computation Jerusalem, Israel
                [6 ]Saint James School of Medicine Plaza Juliana, Kralendijk, Bonaire, Dutch Caribbean, The Netherlands
                [7 ]Neuropsychiatric Disorders Group, Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences Amsterdam, The Netherlands
                Author notes
                * Corresponding author: Tel: +32 16 373 101; Fax: +32 16 330 827; E-mail: bart.destrooper@ 123456cme.vib-kuleuven.be
                Article
                DOI: 10.1002/emmm.201201974
                PMC ID: 3799583
                PubMed ID: 24014289
                SO-VID: 76c8517c-add9-4679-a623-5ed7c1c483f9
                Copyright © © 2013 The Authors. Published by John Wiley and Sons, Ltd on behalf of EMBO
                License:

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

                History
                Date received : 03 September 2012
                Date revision received : 25 July 2013
                Date accepted : 26 July 2013
                Categories
                Subject: Research Articles

                ScienceOpen disciplines: Molecular medicine
                Keywords: alzheimer's disease,hippocampus,prefrontal cortex,microrna,mir-132-3p
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: alzheimer's disease, hippocampus, prefrontal cortex, microrna, mir-132-3p

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