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The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent

Vascular brain pathology constitutes a common feature in neurodegenerative diseases that could underlie their development. Indeed, vascular dysfunction acts synergistically with neurodegenerative changes to exacerbate the cognitive impairment found in Alzheimer’s disease. Different injuries such as...

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Autores principales: Frontiñán-Rubio, Javier, Rabanal-Ruiz, Yoana, Durán-Prado, Mario, Alcain, Francisco Javier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8615161/
https://www.ncbi.nlm.nih.gov/pubmed/34829677
http://dx.doi.org/10.3390/antiox10111806
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author Frontiñán-Rubio, Javier
Rabanal-Ruiz, Yoana
Durán-Prado, Mario
Alcain, Francisco Javier
author_facet Frontiñán-Rubio, Javier
Rabanal-Ruiz, Yoana
Durán-Prado, Mario
Alcain, Francisco Javier
author_sort Frontiñán-Rubio, Javier
collection PubMed
description Vascular brain pathology constitutes a common feature in neurodegenerative diseases that could underlie their development. Indeed, vascular dysfunction acts synergistically with neurodegenerative changes to exacerbate the cognitive impairment found in Alzheimer’s disease. Different injuries such as hypertension, high glucose, atherosclerosis associated with oxidized low-density lipoprotein or inflammation induce NADPH oxidase activation, overproduction of reactive oxygen species, and apoptosis in endothelial cells. Since it has been shown that pretreatment of cultured endothelial cells with the lipophilic antioxidant coenzyme Q10 (CoQ10) displays a protective effect against the deleterious injuries caused by different agents, this study explores the cytoprotective role of different CoQs homologues against Aβ(25–35)-induced damage and demonstrates that only pretreatment with CoQ10 protects endothelial brain cells from Aβ(25–35)-induced damage. Herein, we show that CoQ10 constitutes the most effective ubiquinone in preventing NADPH oxidase activity and reducing both reactive oxygen species generation and the increase in free cytosolic Ca(2+) induced by Aβ(25–35), ultimately preventing apoptosis and necrosis. The specific cytoprotective effect of CoQ with a side chain of 10 isoprenoid units could be explained by the fact that CoQ10 is the only ubiquinone that significantly reduces the entry of Aβ(25–35) into the mitochondria.
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spelling pubmed-86151612021-11-26 The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent Frontiñán-Rubio, Javier Rabanal-Ruiz, Yoana Durán-Prado, Mario Alcain, Francisco Javier Antioxidants (Basel) Article Vascular brain pathology constitutes a common feature in neurodegenerative diseases that could underlie their development. Indeed, vascular dysfunction acts synergistically with neurodegenerative changes to exacerbate the cognitive impairment found in Alzheimer’s disease. Different injuries such as hypertension, high glucose, atherosclerosis associated with oxidized low-density lipoprotein or inflammation induce NADPH oxidase activation, overproduction of reactive oxygen species, and apoptosis in endothelial cells. Since it has been shown that pretreatment of cultured endothelial cells with the lipophilic antioxidant coenzyme Q10 (CoQ10) displays a protective effect against the deleterious injuries caused by different agents, this study explores the cytoprotective role of different CoQs homologues against Aβ(25–35)-induced damage and demonstrates that only pretreatment with CoQ10 protects endothelial brain cells from Aβ(25–35)-induced damage. Herein, we show that CoQ10 constitutes the most effective ubiquinone in preventing NADPH oxidase activity and reducing both reactive oxygen species generation and the increase in free cytosolic Ca(2+) induced by Aβ(25–35), ultimately preventing apoptosis and necrosis. The specific cytoprotective effect of CoQ with a side chain of 10 isoprenoid units could be explained by the fact that CoQ10 is the only ubiquinone that significantly reduces the entry of Aβ(25–35) into the mitochondria. MDPI 2021-11-13 /pmc/articles/PMC8615161/ /pubmed/34829677 http://dx.doi.org/10.3390/antiox10111806 Text en © 2021 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
Frontiñán-Rubio, Javier
Rabanal-Ruiz, Yoana
Durán-Prado, Mario
Alcain, Francisco Javier
The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
title The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
title_full The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
title_fullStr The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
title_full_unstemmed The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
title_short The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
title_sort protective effect of ubiquinone against the amyloid peptide in endothelial cells is isoprenoid chain length-dependent
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8615161/
https://www.ncbi.nlm.nih.gov/pubmed/34829677
http://dx.doi.org/10.3390/antiox10111806
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