A Primeval Mechanism of Tolerance to Desiccation Based on Glycolic Acid Saves Neurons in Mammals from Ischemia by Reducing Intracellular Calcium‐Mediated Excitotoxicity

Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia‐induced damage that occurs before reperfusion or neuronal damage induced by ischemia...

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Published inAdvanced science Vol. 9; no. 4; pp. e2103265 - n/a
Main Authors Chovsepian, Alexandra, Berchtold, Daniel, Winek, Katarzyna, Mamrak, Uta, Ramírez Álvarez, Inés, Dening, Yanina, Golubczyk, Dominika, Weitbrecht, Luis, Dames, Claudia, Aillery, Marine, Fernandez‐Sanz, Celia, Gajewski, Zdzislaw, Dieterich, Marianne, Janowski, Miroslaw, Falkai, Peter, Walczak, Piotr, Plesnila, Nikolaus, Meisel, Andreas, Pan‐Montojo, Francisco
Format Journal Article
LanguageEnglish
Published Germany John Wiley & Sons, Inc 01.02.2022
John Wiley and Sons Inc
Wiley
Subjects
Acids
Apoptosis
Free radicals
Glucose
glutamate‐dependent excitotoxicity
Ischemia
ischemia–reperfusion damage
Metabolism
neuroprotection
Stroke
Variance analysis
glutamate-dependent excitotoxicity
Stroke
ischemia-reperfusion damage
neuroprotection
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Abstract Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia‐induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate‐dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients. In this paper, it is shown how the survival strategy of the worm Caenorhabditis elegans against desiccation, namely, producing glycolic acid at high concentrations, can be used to protect against stroke in mammals. Glycolic acid mitigates the deleterious effects of ischemia/reperfusion by decreasing the glutamate‐dependent abnormal calcium influx to the cells, leading to reduced lesion sizes in mice and swine.
AbstractList Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia‐induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate‐dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients.
Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia-induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate-dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients.
Abstract Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia‐induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate‐dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients.
Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia-induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate-dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients.Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia-induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate-dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients.
Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia‐induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate‐dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients. In this paper, it is shown how the survival strategy of the worm Caenorhabditis elegans against desiccation, namely, producing glycolic acid at high concentrations, can be used to protect against stroke in mammals. Glycolic acid mitigates the deleterious effects of ischemia/reperfusion by decreasing the glutamate‐dependent abnormal calcium influx to the cells, leading to reduced lesion sizes in mice and swine.
Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia‐induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate‐dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients. In this paper, it is shown how the survival strategy of the worm Caenorhabditis elegans against desiccation, namely, producing glycolic acid at high concentrations, can be used to protect against stroke in mammals. Glycolic acid mitigates the deleterious effects of ischemia/reperfusion by decreasing the glutamate‐dependent abnormal calcium influx to the cells, leading to reduced lesion sizes in mice and swine.
Author Dames, Claudia
Aillery, Marine
Berchtold, Daniel
Chovsepian, Alexandra
Golubczyk, Dominika
Fernandez‐Sanz, Celia
Walczak, Piotr
Janowski, Miroslaw
Dening, Yanina
Winek, Katarzyna
Falkai, Peter
Ramírez Álvarez, Inés
Dieterich, Marianne
Gajewski, Zdzislaw
Meisel, Andreas
Weitbrecht, Luis
Pan‐Montojo, Francisco
Plesnila, Nikolaus
Mamrak, Uta
AuthorAffiliation 3 Laboratory of Experimental Stroke Research Institute for Stroke and Dementia Research (ISD) University of Munich Medical Center Feodor‐Lynen‐Strasse 17 81377 Munich Germany
4 Department of Neurology Ludwig‐Maximilian University Hospital Marchioninstrasse. 15 81377 Munich Germany
5 Munich Cluster for Systems Neurology (SyNergy) Ludwig‐Maximilian University Munich 81377 Munich Germany
7 Center for Translational Medicine Warsaw University of Life Sciences Warsaw 02‐787 Poland
10 Present address: Present address: Seppic Île‐de‐France La Garenne‐Colombes 92250 France
11 Present address: Present address: Center for Translational Medicine Department of Medicine Thomas Jefferson University Philadelphia PA 19107 USA
2 Department of Neurology NeuroCure Clinical Research Center Center for Stroke Research Charité University Medicine Charitéplatz 1 10117 Berlin Germany
8 Program in Image Guided Neurointerventions Department of Diagnostic Radiology and Nuclear Medicine University of Maryland Baltimore MD
AuthorAffiliation_xml – name: 8 Program in Image Guided Neurointerventions Department of Diagnostic Radiology and Nuclear Medicine University of Maryland Baltimore MD 21201 USA
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– name: 4 Department of Neurology Ludwig‐Maximilian University Hospital Marchioninstrasse. 15 81377 Munich Germany
– name: 6 Ti‐com LLC Trylinskiego 2 Olsztyn 10‐683 Poland
– name: 10 Present address: Present address: Seppic Île‐de‐France La Garenne‐Colombes 92250 France
– name: 9 Present address: Present address: Edmond and Lily Safra Center for Brain Sciences Hebrew University of Jerusalem Jerusalem 9190401 Israel
– name: 2 Department of Neurology NeuroCure Clinical Research Center Center for Stroke Research Charité University Medicine Charitéplatz 1 10117 Berlin Germany
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34904402$$D View this record in MEDLINE/PubMed
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Issue 4
Keywords glutamate-dependent excitotoxicity
Stroke
ischemia-reperfusion damage
neuroprotection
Language English
License Attribution
2021 The Authors. Advanced Science published by Wiley-VCH GmbH.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Snippet Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy,...
Abstract Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical...
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StartPage e2103265
SubjectTerms Acids
Apoptosis
Free radicals
Glucose
glutamate‐dependent excitotoxicity
Ischemia
ischemia–reperfusion damage
Metabolism
neuroprotection
Stroke
Variance analysis
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Title A Primeval Mechanism of Tolerance to Desiccation Based on Glycolic Acid Saves Neurons in Mammals from Ischemia by Reducing Intracellular Calcium‐Mediated Excitotoxicity
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