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...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Javier Frontiñán-Rubio, Yoana Rabanal-Ruiz, Mario Durán-Prado, Francisco Javier Alcain
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	Alzheimer´s disease coenzyme Q ubiquinol NADPH oxidase amyloid beta endothelial cells Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/92fbebc4702d41b688e4eca062faa3df
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:92fbebc4702d41b688e4eca062faa3df
record_format	dspace
spelling	oai:doaj.org-article:92fbebc4702d41b688e4eca062faa3df2021-11-25T16:28:52ZThe Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent10.3390/antiox101118062076-3921https://doaj.org/article/92fbebc4702d41b688e4eca062faa3df2021-11-01T00:00:00Zhttps://www.mdpi.com/2076-3921/10/11/1806https://doaj.org/toc/2076-3921Vascular 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<sub>25–35</sub>-induced damage and demonstrates that only pretreatment with CoQ10 protects endothelial brain cells from Aβ<sub>25–35</sub>-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<sup>2+</sup> induced by Aβ<sub>25–35</sub>, 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<sub>25–35</sub> into the mitochondria.Javier Frontiñán-RubioYoana Rabanal-RuizMario Durán-PradoFrancisco Javier AlcainMDPI AGarticleAlzheimer´s diseasecoenzyme QubiquinolNADPH oxidaseamyloid betaendothelial cellsTherapeutics. PharmacologyRM1-950ENAntioxidants, Vol 10, Iss 1806, p 1806 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Alzheimer´s disease coenzyme Q ubiquinol NADPH oxidase amyloid beta endothelial cells Therapeutics. Pharmacology RM1-950
spellingShingle	Alzheimer´s disease coenzyme Q ubiquinol NADPH oxidase amyloid beta endothelial cells Therapeutics. Pharmacology RM1-950 Javier Frontiñán-Rubio Yoana Rabanal-Ruiz Mario Durán-Prado Francisco Javier Alcain The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent
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<sub>25–35</sub>-induced damage and demonstrates that only pretreatment with CoQ10 protects endothelial brain cells from Aβ<sub>25–35</sub>-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<sup>2+</sup> induced by Aβ<sub>25–35</sub>, 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<sub>25–35</sub> into the mitochondria.
format	article
author	Javier Frontiñán-Rubio Yoana Rabanal-Ruiz Mario Durán-Prado Francisco Javier Alcain
author_facet	Javier Frontiñán-Rubio Yoana Rabanal-Ruiz Mario Durán-Prado Francisco Javier Alcain
author_sort	Javier Frontiñán-Rubio
title	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_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_sort	protective effect of ubiquinone against the amyloid peptide in endothelial cells is isoprenoid chain length-dependent
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/92fbebc4702d41b688e4eca062faa3df
work_keys_str_mv	AT javierfrontinanrubio theprotectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT yoanarabanalruiz theprotectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT marioduranprado theprotectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT franciscojavieralcain theprotectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT javierfrontinanrubio protectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT yoanarabanalruiz protectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT marioduranprado protectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent AT franciscojavieralcain protectiveeffectofubiquinoneagainsttheamyloidpeptideinendothelialcellsisisoprenoidchainlengthdependent
_version_	1718413150957600768

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

Ejemplares similares