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      Promising targets of cell death signaling of NR2B receptor subunit in stroke pathogenesis

      , ,
      Regenerative Medicine Research
      BioMed Central
      Stroke, DAPK1, NMDA receptor, Neuronal death

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          Stroke is an acute cerebrovascular disease caused by acute brain artery bursting or cerebral embolism that leads to neuronal death and severe dysfunction of synaptic transmission. Neuronal damage after stroke remains a major cause of morbidity and mortality worldwide and affects 795 000 of lives every year in United States. However, effective treatments remain lacking, which makes the identification of new therapeutic targets a matter of great importance.

          N-methyl-D-aspartate glutamate (NMDA) receptor is important both in the normal synaptic transmission and in the neuronal death after stroke. Accumulated evidences show NMDA receptor downstream effectors, such as PSD-95, DAPK1, and ERK, had been revealed to be linked with neuronal damage. Based on our recent studies, we review the promising targets of the NMDA receptor downstream signaling involved in stroke treatment. This review will provide the concept of NR2B downstream signaling in neuronal death after stroke and provide evidences for developing better NMDAR-based therapeutics by targeting downstream proteins.

          Most cited references43

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          The glutamate receptor ion channels.

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            NMDA receptor subunits: diversity, development and disease

            Current Opinion in Neurobiology, 11(3), 327-335
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              Reactive astrocytes: cellular and molecular cues to biological function.

              For several decades, the reactive gliosis that occurs after an injury to the CNS has been considered one of the major impediments to axonal regeneration. Nevertheless, recent studies have suggested that in certain conditions, reactive astrocytes may provide a permissive substratum to support axonal regrowth. The important criteria, allowing for the distinction between permissive and non-permissive gliosis, are the ultrastructural 3D organization of the scar and more importantly the recognition molecules expressed by reactive astrocytes. Reactive astrocytes express surface molecules and produce various neurotrophic factors and cytokines. The latter in turn might modulate the production of recognition molecules by reactive astrocytes, allowing them to support post-lesional axonal regrowth. Although numerous recent articles have focused on cytokines and cell adhesion molecules, scant attention has been paid to reactive astrocytes. Reactive astrocytes should be considered a key element, like neurons, of a dynamic environment, thus forming with neurons a functional unit involved in homeostasis, plasticity and neurotransmission. Attempts are in progress to identify molecular markers for reactive astrocytes.

                Author and article information

                Regen Med Res
                Regen Med Res
                Regenerative Medicine Research
                BioMed Central (London )
                23 July 2014
                23 July 2014
                December 2014
                : 2
                : 1
                : 8
                Department of Pathophysiology, Tongji Medical College and Institute for Brain Research, Huazhong University of Science and Technology, 13# Hangkong Road, Wuhan, 430030 PR China
                © Shu et al.; licensee BioMed Central Ltd. 2014

                This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                : 15 March 2014
                : 10 July 2014
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                © The Author(s) 2014

                stroke,dapk1,nmda receptor,neuronal death
                stroke, dapk1, nmda receptor, neuronal death


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