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      Regulation of Injury-Induced Neurogenesis by Nitric Oxide

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          Abstract

          The finding that neural stem cells (NSCs) are able to divide, migrate, and differentiate into several cellular types in the adult brain raised a new hope for restorative neurology. Nitric oxide (NO), a pleiotropic signaling molecule in the central nervous system (CNS), has been described to be able to modulate neurogenesis, acting as a pro- or antineurogenic agent. Some authors suggest that NO is a physiological inhibitor of neurogenesis, while others described NO to favor neurogenesis, particularly under inflammatory conditions. Thus, targeting the NO system may be a powerful strategy to control the formation of new neurons. However, the exact mechanisms by which NO regulates neural proliferation and differentiation are not yet completely clarified. In this paper we will discuss the potential interest of the modulation of the NO system for the treatment of neurodegenerative diseases or other pathological conditions that may affect the CNS.

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          Neuronal replacement from endogenous precursors in the adult brain after stroke.

          Andreas Arvidsson, Tove Collin, Deniz Kirik … (2002)
          In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we show that the adult brain has the capacity for self-repair after insults causing extensive neuronal death. If the new neurons are functional and their formation can be stimulated, a novel therapeutic strategy might be developed for stroke in humans.
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            Inflammation in neurodegenerative disease--a double-edged sword.

            Tony Wyss-Coray, Lennart Mucke (2002)
            Inflammation is a defense reaction against diverse insults, designed to remove noxious agents and to inhibit their detrimental effects. It consists of a dazzling array of molecular and cellular mechanisms and an intricate network of controls to keep them in check. In neurodegenerative diseases, inflammation may be triggered by the accumulation of proteins with abnormal conformations or by signals emanating from injured neurons. Given the multiple functions of many inflammatory factors, it has been difficult to pinpoint their roles in specific (patho)physiological situations. Studies of genetically modified mice and of molecular pathways in activated glia are beginning to shed light on this issue. Altered expression of different inflammatory factors can either promote or counteract neurodegenerative processes. Since many inflammatory responses are beneficial, directing and instructing the inflammatory machinery may be a better therapeutic objective than suppressing it.
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              Nitric oxide synthases: roles, tolls, and controls.

              Carl Nathan, Qiao-wen Xie (1994)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Stem Cells Int
                Journal ID (iso-abbrev): Stem Cells Int
                Journal ID (publisher-id): SCI
                Title: Stem Cells International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1687-966X
                ISSN (Electronic): 1687-9678
                Publication date (Print): 2012
                Publication date (Electronic): 10 September 2012
                Volume: 2012
                Electronic Location Identifier: 895659
                Affiliations
                1Centre for Neuroscience and Cell Biology, Neuroendocrinology and Neurogenesis Group, University of Coimbra, Coimbra, Portugal
                2Regenerative Medicine Program, Department of Biomedical Sciences and Medicine, Gambelas Campus, University of Algarve, 8005-139 Faro, Portugal
                3IBB-Institute for Biotechnology and Bioengineering, Centre of Molecular and Structural Biomedicine, Gambelas Campus, University of Algarve, 8005-139 Faro, Portugal
                Author notes
                *Inês M. Araújo: imaraujo@ 123456ualg.pt

                Academic Editor: Oscar Gonzalez-Perez

                Article
                DOI: 10.1155/2012/895659
                PMC ID: 3444935
                PubMed ID: 22997523
                SO-VID: 0bee4949-d558-4868-a8d2-38371c2548de
                Copyright © Copyright © 2012 Bruno P. Carreira et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 June 2012
                Date accepted : 19 July 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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