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Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II
The increase of vascular arginase activity during aging causes endothelial dysfunction. This enzyme competes with the endothelial nitric oxide synthase (eNOS) for L-arginine substrate. Our hypothesis is that glucose 6-P dehydrogenase (G6PD) overexpression could improve the endothelial function modul...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9961129/ https://www.ncbi.nlm.nih.gov/pubmed/36835034 http://dx.doi.org/10.3390/ijms24043622 |
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author | Serna, Eva Mauricio, Maria D San-Miguel, Teresa Guerra-Ojeda, Sol Verdú, David Valls, Alicia Arc-Chagnaud, Coralie De la Rosa, Adrián Viña, José |
author_facet | Serna, Eva Mauricio, Maria D San-Miguel, Teresa Guerra-Ojeda, Sol Verdú, David Valls, Alicia Arc-Chagnaud, Coralie De la Rosa, Adrián Viña, José |
author_sort | Serna, Eva |
collection | PubMed |
description | The increase of vascular arginase activity during aging causes endothelial dysfunction. This enzyme competes with the endothelial nitric oxide synthase (eNOS) for L-arginine substrate. Our hypothesis is that glucose 6-P dehydrogenase (G6PD) overexpression could improve the endothelial function modulating the arginase pathway in aorta from mice. For this study, three groups of male mice were used: young wild type (WT) (6–9 months), old WT (21–22 months) and old G6PD-Tg (21–22 months) mice. Vascular reactivity results showed a reduced acetylcholine-dependent relaxation in the old WT but not old G6PD-Tg group. Endothelial dysfunction was reverted by nor-NOHA, an arginase inhibitor. Mice overexpressing G6PD underexpressed arginase II and also displayed a lower activity of this enzyme. Moreover, histological analyses demonstrated that age causes a thickness of aortic walls, but this did not occur in G6PD-Tg mice. We conclude that the overexpressing G6PD mouse is a model to improve vascular health via the arginase pathway. |
format | Online Article Text |
id | pubmed-9961129 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99611292023-02-26 Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II Serna, Eva Mauricio, Maria D San-Miguel, Teresa Guerra-Ojeda, Sol Verdú, David Valls, Alicia Arc-Chagnaud, Coralie De la Rosa, Adrián Viña, José Int J Mol Sci Article The increase of vascular arginase activity during aging causes endothelial dysfunction. This enzyme competes with the endothelial nitric oxide synthase (eNOS) for L-arginine substrate. Our hypothesis is that glucose 6-P dehydrogenase (G6PD) overexpression could improve the endothelial function modulating the arginase pathway in aorta from mice. For this study, three groups of male mice were used: young wild type (WT) (6–9 months), old WT (21–22 months) and old G6PD-Tg (21–22 months) mice. Vascular reactivity results showed a reduced acetylcholine-dependent relaxation in the old WT but not old G6PD-Tg group. Endothelial dysfunction was reverted by nor-NOHA, an arginase inhibitor. Mice overexpressing G6PD underexpressed arginase II and also displayed a lower activity of this enzyme. Moreover, histological analyses demonstrated that age causes a thickness of aortic walls, but this did not occur in G6PD-Tg mice. We conclude that the overexpressing G6PD mouse is a model to improve vascular health via the arginase pathway. MDPI 2023-02-11 /pmc/articles/PMC9961129/ /pubmed/36835034 http://dx.doi.org/10.3390/ijms24043622 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Serna, Eva Mauricio, Maria D San-Miguel, Teresa Guerra-Ojeda, Sol Verdú, David Valls, Alicia Arc-Chagnaud, Coralie De la Rosa, Adrián Viña, José Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II |
title | Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II |
title_full | Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II |
title_fullStr | Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II |
title_full_unstemmed | Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II |
title_short | Glucose 6-P Dehydrogenase Overexpression Improves Aging-Induced Endothelial Dysfunction in Aorta from Mice: Role of Arginase II |
title_sort | glucose 6-p dehydrogenase overexpression improves aging-induced endothelial dysfunction in aorta from mice: role of arginase ii |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9961129/ https://www.ncbi.nlm.nih.gov/pubmed/36835034 http://dx.doi.org/10.3390/ijms24043622 |
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