Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration
Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thu...
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| Published in | PLoS biology Vol. 8; no. 9; p. e1000479 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.09.2010
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1545-7885 1544-9173 1545-7885 |
| DOI | 10.1371/journal.pbio.1000479 |
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| Abstract | Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4(-/-)) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4(-/-) mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. |
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| AbstractList | Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4(-/-)) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4(-/-) mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. The identification of NOX4 as a major source of oxidative stress in stroke and demonstration of dramatic protection after stroke in mice by NOX4 deletion or NOX inhibition, opens up new avenues for treatment. Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 ( Nox4 −/− ) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4 −/− mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. Stroke is the second leading cause of death worldwide. Today, only one approved therapy exists—a drug that breaks down blood clots—the effectiveness of which is moderate, and it can only be used in about 10% of patients because of contraindications. New therapeutic strategies that are translatable to humans and more rigid thresholds of relevance in pre-clinical stroke models are needed. One candidate mechanism is oxidative stress, which is the damage caused by reactive oxygen species (ROS). Antioxidant approaches that specifically target ROS have thus far failed in clinical trials. For a more effective approach, we focus here on targeting ROS at its source by investigating an enzyme involved in generating ROS, known as NADPH oxidase type 4, or NOX4. We found that NOX4 causes oxidative stress and death of nerve cells after a stroke. Deletion of the NOX4-coding gene in mice, as well as inhibiting the ROS-generating activity of NOX with a pharmacological inhibitor, reduces brain damage and improves neurological function, even when given hours after a stroke. Importantly, neuroprotection was preserved in old male and female Nox4 −/− mice as well as in Nox4 −/− mice subjected to permanent ischemia. NOX4 thus represents a most promising new therapeutic target for reducing oxidative stress in general, and in brain injury due to stroke in particular. Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4-/-) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4-/- mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 ([Nox4.sup.-/-]) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke- protective phenotype in [Nox4.sup.-/-] mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4(-/-)) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4(-/-) mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy.Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4(-/-)) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4(-/-) mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. |
| Audience | Academic |
| Author | Shah, Ajay M. Wingler, Kirstin Grund, Henrike Weissmann, Norbert Meuth, Sven G. de Angelis, Martin Hrabé Barit, David Schuhmann, Michael K. Schwarz, Tobias Barthel, Konstanze Stoll, Guido Herrmann, Alexander M. Becker, Lore Kleinschnitz, Christoph Meurer, Sabine Schmidt, Harald H. H. W. Mittal, Manish Jones, Emma Schrewe, Anja Klopstock, Thomas Fuchs, Helmut Gailus-Durner, Valérie Kraft, Peter Geis, Christian Armitage, Melanie E. Jandeleit-Dahm, Karin |
| AuthorAffiliation | University of Edinburgh, United Kingdom 6 Baker IDI Heart and Diabetes Institute, Juvenile Diabetes Research Foundation (JDRF) International Center for Diabetic Complications Research, Melbourne, Australia 5 National Stroke Research Institute, Florey Neuroscience Institutes, Melbourne, Australia 7 Abteilung Neurologie, Georg-August Universität Göttingen, Göttingen, Germany 10 Friedrich-Baur-Institut an der Neurologischen Klinik, Klinikum der Ludwig-Maximilians-Universität München, München, Germany 1 Neurologische Klinik und Poliklinik, Universität Würzburg, Würzburg, Germany 8 Universitätsklinik Münster, Klinik und Poliklinik für Neurologie—Entzündliche Erkrankungen des Nervensystems und Neuroonkologie, Münster, Germany 11 Lehrstuhl für Experimentelle Genetik, Technische Universität München, Freising-Weihenstephan, Germany 4 Department of Pharmacology and Toxicology and Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, The Netherlands 3 Department of Pharmacology and |
| AuthorAffiliation_xml | – name: 2 Rudolf-Buchheim-Institut für Pharmakologie & Medizinische Klinik, Justus-Liebig-Universität, Gießen, Germany – name: 4 Department of Pharmacology and Toxicology and Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, The Netherlands – name: 6 Baker IDI Heart and Diabetes Institute, Juvenile Diabetes Research Foundation (JDRF) International Center for Diabetic Complications Research, Melbourne, Australia – name: 9 Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, München, Germany – name: 3 Department of Pharmacology and Centre for Vascular Health, Monash University, Melbourne, Australia – name: 10 Friedrich-Baur-Institut an der Neurologischen Klinik, Klinikum der Ludwig-Maximilians-Universität München, München, Germany – name: 8 Universitätsklinik Münster, Klinik und Poliklinik für Neurologie—Entzündliche Erkrankungen des Nervensystems und Neuroonkologie, Münster, Germany – name: 7 Abteilung Neurologie, Georg-August Universität Göttingen, Göttingen, Germany – name: University of Edinburgh, United Kingdom – name: 12 King's College London School of Medicine, The James Black Centre, Cardiovascular Division, London, United Kingdom – name: 5 National Stroke Research Institute, Florey Neuroscience Institutes, Melbourne, Australia – name: 11 Lehrstuhl für Experimentelle Genetik, Technische Universität München, Freising-Weihenstephan, Germany – name: 1 Neurologische Klinik und Poliklinik, Universität Würzburg, Würzburg, Germany |
| Author_xml | – sequence: 1 givenname: Christoph surname: Kleinschnitz fullname: Kleinschnitz, Christoph – sequence: 2 givenname: Henrike surname: Grund fullname: Grund, Henrike – sequence: 3 givenname: Kirstin surname: Wingler fullname: Wingler, Kirstin – sequence: 4 givenname: Melanie E. surname: Armitage fullname: Armitage, Melanie E. – sequence: 5 givenname: Emma surname: Jones fullname: Jones, Emma – sequence: 6 givenname: Manish surname: Mittal fullname: Mittal, Manish – sequence: 7 givenname: David surname: Barit fullname: Barit, David – sequence: 8 givenname: Tobias surname: Schwarz fullname: Schwarz, Tobias – sequence: 9 givenname: Christian surname: Geis fullname: Geis, Christian – sequence: 10 givenname: Peter surname: Kraft fullname: Kraft, Peter – sequence: 11 givenname: Konstanze surname: Barthel fullname: Barthel, Konstanze – sequence: 12 givenname: Michael K. surname: Schuhmann fullname: Schuhmann, Michael K. – sequence: 13 givenname: Alexander M. surname: Herrmann fullname: Herrmann, Alexander M. – sequence: 14 givenname: Sven G. surname: Meuth fullname: Meuth, Sven G. – sequence: 15 givenname: Guido surname: Stoll fullname: Stoll, Guido – sequence: 16 givenname: Sabine surname: Meurer fullname: Meurer, Sabine – sequence: 17 givenname: Anja surname: Schrewe fullname: Schrewe, Anja – sequence: 18 givenname: Lore surname: Becker fullname: Becker, Lore – sequence: 19 givenname: Valérie surname: Gailus-Durner fullname: Gailus-Durner, Valérie – sequence: 20 givenname: Helmut surname: Fuchs fullname: Fuchs, Helmut – sequence: 21 givenname: Thomas surname: Klopstock fullname: Klopstock, Thomas – sequence: 22 givenname: Martin Hrabé surname: de Angelis fullname: de Angelis, Martin Hrabé – sequence: 23 givenname: Karin surname: Jandeleit-Dahm fullname: Jandeleit-Dahm, Karin – sequence: 24 givenname: Ajay M. surname: Shah fullname: Shah, Ajay M. – sequence: 25 givenname: Norbert surname: Weissmann fullname: Weissmann, Norbert – sequence: 26 givenname: Harald H. H. W. surname: Schmidt fullname: Schmidt, Harald H. H. W. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20877715$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2010 Public Library of Science Kleinschnitz et al. 2010 2010 Kleinschnitz 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: Kleinschnitz C, Grund H, Wingler K, Armitage ME, Jones E, et al. (2010) Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration. PLoS Biol 8(9): e1000479. doi:10.1371/journal.pbio.1000479 |
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| Keywords | Brain Phenotype Stroke Animals Reactive Oxygen Species Oxidative Stress Female Male Mice Blood-Brain Barrier Mice, Knockout NADPH Oxidase |
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| Snippet | Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of... The identification of NOX4 as a major source of oxidative stress in stroke and demonstration of dramatic protection after stroke in mice by NOX4 deletion or... Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90%... |
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| SubjectTerms | Animals Antioxidants Blood clots Blood-Brain Barrier Brain - metabolism Brain - pathology Brain damage Cardiovascular Disorders/Cardiovascular Pharmacology Colleges & universities Drug therapy Female Genetics and Genomics/Gene Function Health aspects Ischemia Male Mice Mice, Knockout Mortality NADPH Oxidase 4 NADPH Oxidases - antagonists & inhibitors NADPH Oxidases - genetics NADPH Oxidases - metabolism Neurodegeneration Neurological Disorders/Cerebrovascular Disease Neurological Disorders/Neuropharmacology Nitric oxide Non-Clinical Medicine/Research Methods Oxidases Oxidative Stress Pharmacology/Drug Development Phenotype Physiology/Cardiovascular Physiology and Circulation Prevention Reactive Oxygen Species - metabolism Stroke Stroke (Disease) Stroke - enzymology Stroke - metabolism Stroke - pathology Veins & arteries |
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| Title | Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration |
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