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      Sodium-Dependent Vitamin C Transporter 2 (SVCT2) Expression and Activity in Brain Capillary Endothelial Cells after Transient Ischemia in Mice

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          Abstract

          Expression and transport activity of Sodium-dependent Vitamin C Transporter 2 (SVCT2) was shown in various tissues and organs. Vitamin C was shown to be cerebroprotective in several animal models of stroke. Data on expression, localization and transport activity of SVCT2 after cerebral ischemia, however, has been scarce so far. Thus, we studied the expression of SVCT2 after middle cerebral artery occlusion (MCAO) in mice by immunohistochemistry. We found an upregulation of SVCT2 after stroke. Co-stainings with Occludin, Von-Willebrand Factor and CD34 demonstrated localization of SVCT2 in brain capillary endothelial cells in the ischemic area after stroke. Time-course analyses of SVCT2 expression by immunohistochemistry and western blots showed upregulation in the subacute phase of 2–5 days. Radioactive uptake assays using 14C-labelled ascorbic acid showed a significant increase of ascorbic acid uptake into the brain after stroke. Taken together, these results provide evidence for the expression and transport activity of SVCT2 in brain capillary endothelial cells after transient ischemia in mice. These results may lead to the development of novel neuroprotective strategies in stroke therapy.

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          Pathobiology of ischaemic stroke: an integrated view.

          C Iadecola, M Moskowitz (1999)
          Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from a complex series of pathophysiological events that evolve in time and space. In this article, the relevance of excitotoxicity, peri-infarct depolarizations, inflammation and apoptosis to delayed mechanisms of damage within the peri-infarct zone or ischaemic penumbra are discussed. While focusing on potentially new avenues of treatment, the issue of why many clinical stroke trials have so far proved disappointing is addressed. This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.
          Article 0 comments Cited 293 times – based on 0 reviews     Review now
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            Predictors of in-hospital mortality and attributable risks of death after ischemic stroke: the German Stroke Registers Study Group.

            R Janzen, Peter U. Heuschmann, Joachim Röther … (2004)
            There is a lack of information about factors associated with in-hospital death and the impact of neurological complications on early outcome for patients with stroke treated in community settings. We investigated predictors for in-hospital mortality and attributable risks of death after ischemic stroke in a pooled analysis of large German stroke registers. Stroke patients admitted to hospitals cooperating within the German Stroke Registers Study Group (ADSR) between January 1, 2000, and December 31, 2000, were analyzed. The ADSR is a network of regional stroke registers, combining data from 104 academic and community hospitals throughout Germany. The impact of patients' demographic and clinical characteristics, their comorbid conditions, and the treating hospital expertise in stroke care on in-hospital mortality was analyzed using Cox regression analysis. Attributable risks of death for medical and neurological complications were calculated. A total of 13 440 ischemic stroke patients were included. Overall in-hospital mortality was 4.9%. In women, higher age (P<.001), severity of stroke defined by number of neurological deficits (P<.001), and atrial fibrillation (hazard ratio [HR], 1.3; 95% confidence interval [CI], 1.0-1.6) were independent predictors for in-hospital death. In men, diabetes (HR, 1.3; 95% CI, 1.0-1.8) and previous stroke (HR 1.4; 95% CI, 1.0-1.9) had a significant negative impact on early outcome in addition to the factors identified for women. The complication with the highest attributable risk proportion was increased intracranial pressure, accounting for 94% (95% CI, 93.9%-94.1%) of deaths among patients with this complication. Pneumonia was the complication with the highest attributable proportion of death in the entire stroke population, accounting for 31.2% (95% CI, 30.9%-31.5%) of all deaths. More than 50% of all in-hospital deaths were caused by serious medical or neurological complications (54.4%; 95% CI, 54.3%-54.5%). Substantial differences were found in the impact of comorbid conditions on early outcome for men and women. Programs aiming at an improvement in short-term outcome after stroke should focus especially on a reduction of pneumonia and an early treatment of increased intracranial pressure.
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              Glucose transporter proteins in brain.

              S Vannucci, Alexander Simpson, F Maher (1994)
              Glucose is the principal energy source for the mammalian brain. The presence of glucose transport proteins is essential to supply glucose to the neurons and glia within the brain. At least three glucose transporter isoforms have now been identified, and are thought to play a significant role, in the brain. This review describes our current understanding of cell-specific glucose transporter expression in brain, which includes GLUT1 (55-kDa form) present at a high concentration at the blood-brain barrier as well as in parenchymal cells (45-kDa form), most likely in astrocytes, GLUT3 expressed in neurons, and GLUT5 in microglia. We discuss some potential implications of this glucose transporter heterogeneity for cerebral metabolic activity.
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                Author and article information

                Contributors
                : Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2011
                Publication date (Electronic): 11 February 2011
                Volume: 6
                Issue: 2
                Electronic Location Identifier: e17139
                Affiliations
                [1 ]Department of Neurology, University Clinic Muenster, Muenster, Germany
                [2 ]Neurologie Bethel, Evangelisches Klinikum Bethel, Bielefeld, Germany
                Biological Research Center of the Hungarian Academy of Sciences, Hungary
                Author notes

                Conceived and designed the experiments: BG PY WRS. Performed the experiments: BG SS. Analyzed the data: BG WRS. Contributed reagents/materials/analysis tools: BG SS JKS PY. Wrote the paper: BG.

                Article
                Publisher ID: PONE-D-10-05184
                DOI: 10.1371/journal.pone.0017139
                PMC ID: 3037964
                PubMed ID: 21347255
                SO-VID: 66fbdd70-4306-41d6-ad46-db00b3a8608b
                Copyright © Gess et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                Date received : 16 November 2010
                Date accepted : 21 January 2011
                Page count
                Pages: 8
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Biochemistry
                Subject: Immunochemistry
                Subject: Immunology
                Subject: Immunologic Techniques
                Subject: Immunohistochemical Analysis
                Subject: Model Organisms
                Subject: Animal Models
                Subject: Mouse
                Subject: Molecular Cell Biology
                Subject: Cellular Types
                Subject: Endothelial Cells
                Subject: Neuroscience
                Subject: Cellular Neuroscience
                Subject: Molecular Neuroscience
                Subject: Medicine
                Subject: Neurology
                Subject: Cerebrovascular Diseases
                Subject: Ischemic Stroke
                Subject: Nutrition
                Subject: Vitamins

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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