NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)

NADPH oxidases (NOX) constitute the main reactive oxygen species (ROS) source in blood vessels. An oxidative stress situation due to ROS overproduction can lead into endothelial dysfunction, a molecular mechanism that precedes cardiovascular diseases (CVDs) such as atherosclerosis, myocardial infarc...
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Autor*in:	Javier Marqués [verfasserIn] Joaquín Fernández-Irigoyen [verfasserIn] Elena Ainzúa [verfasserIn] María Martínez-Azcona [verfasserIn] Adriana Cortés [verfasserIn] Carmen Roncal [verfasserIn] Josune Orbe [verfasserIn] Enrique Santamaría [verfasserIn] Guillermo Zalba [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	NADPH oxidase 5 endothelial cells endothelial dysfunction cell proliferation cell migration mitochondrial dysfunction

Übergeordnetes Werk:	In: Antioxidants - MDPI AG, 2013, 11(2022), 11, p 2147
Übergeordnetes Werk:	volume:11 ; year:2022 ; number:11, p 2147

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/antiox11112147

Katalog-ID:	DOAJ085867357

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language	English
source	In Antioxidants 11(2022), 11, p 2147 volume:11 year:2022 number:11, p 2147
sourceStr	In Antioxidants 11(2022), 11, p 2147 volume:11 year:2022 number:11, p 2147
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topic_facet	NADPH oxidase 5 endothelial cells endothelial dysfunction cell proliferation cell migration mitochondrial dysfunction Therapeutics. Pharmacology
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authorswithroles_txt_mv	Javier Marqués @@aut@@ Joaquín Fernández-Irigoyen @@aut@@ Elena Ainzúa @@aut@@ María Martínez-Azcona @@aut@@ Adriana Cortés @@aut@@ Carmen Roncal @@aut@@ Josune Orbe @@aut@@ Enrique Santamaría @@aut@@ Guillermo Zalba @@aut@@
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callnumber-first	R - Medicine
author	Javier Marqués
spellingShingle	Javier Marqués misc RM1-950 misc NADPH oxidase 5 misc endothelial cells misc endothelial dysfunction misc cell proliferation misc cell migration misc mitochondrial dysfunction misc Therapeutics. Pharmacology NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)
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topic_title	RM1-950 NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3) NADPH oxidase 5 endothelial cells endothelial dysfunction cell proliferation cell migration mitochondrial dysfunction
topic	misc RM1-950 misc NADPH oxidase 5 misc endothelial cells misc endothelial dysfunction misc cell proliferation misc cell migration misc mitochondrial dysfunction misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc NADPH oxidase 5 misc endothelial cells misc endothelial dysfunction misc cell proliferation misc cell migration misc mitochondrial dysfunction misc Therapeutics. Pharmacology
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title	NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)
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title_full	NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)
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title_sort	nadph oxidase 5 (nox5) overexpression promotes endothelial dysfunction via cell apoptosis, migration, and metabolic alterations in human brain microvascular endothelial cells (hcmec/d3)
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title_auth	NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)
abstract	NADPH oxidases (NOX) constitute the main reactive oxygen species (ROS) source in blood vessels. An oxidative stress situation due to ROS overproduction can lead into endothelial dysfunction, a molecular mechanism that precedes cardiovascular diseases (CVDs) such as atherosclerosis, myocardial infarction, and stroke. NOX5 is the last discovered member of the NOX family, studied in a lesser extent due to its absence in the rodent genome. Our objective was to describe the phenotypic alterations produced by an oxidative stress situation derived from NOX5 overexpression in an endothelial in vitro model. The in vitro model consists of the hCMEC/D3 cell line, derived from brain microvascular endothelium, infected with a recombinant NOX5-β adenovirus. After an initial proteomic analysis, three phenotypic alterations detected in silico were studied: cell proliferation and apoptosis, general and mitochondrial metabolism, and migration capacity. NOX5 infection of hCMEC/D3 generates a functional protein and an increase in ROS production. This model produced changes in the whole cell proteome. The in silico analysis together with in vitro validations demonstrated that NOX5 overexpression inhibits proliferation and promotes apoptosis, metabolic alterations and cell migration in hCMEC/D3 cells. NOX5 overexpression in endothelial cells leads to phenotypic changes that can lead to endothelial dysfunction, the onset of atherosclerosis, myocardial infarction, and stroke.
abstractGer	NADPH oxidases (NOX) constitute the main reactive oxygen species (ROS) source in blood vessels. An oxidative stress situation due to ROS overproduction can lead into endothelial dysfunction, a molecular mechanism that precedes cardiovascular diseases (CVDs) such as atherosclerosis, myocardial infarction, and stroke. NOX5 is the last discovered member of the NOX family, studied in a lesser extent due to its absence in the rodent genome. Our objective was to describe the phenotypic alterations produced by an oxidative stress situation derived from NOX5 overexpression in an endothelial in vitro model. The in vitro model consists of the hCMEC/D3 cell line, derived from brain microvascular endothelium, infected with a recombinant NOX5-β adenovirus. After an initial proteomic analysis, three phenotypic alterations detected in silico were studied: cell proliferation and apoptosis, general and mitochondrial metabolism, and migration capacity. NOX5 infection of hCMEC/D3 generates a functional protein and an increase in ROS production. This model produced changes in the whole cell proteome. The in silico analysis together with in vitro validations demonstrated that NOX5 overexpression inhibits proliferation and promotes apoptosis, metabolic alterations and cell migration in hCMEC/D3 cells. NOX5 overexpression in endothelial cells leads to phenotypic changes that can lead to endothelial dysfunction, the onset of atherosclerosis, myocardial infarction, and stroke.
abstract_unstemmed	NADPH oxidases (NOX) constitute the main reactive oxygen species (ROS) source in blood vessels. An oxidative stress situation due to ROS overproduction can lead into endothelial dysfunction, a molecular mechanism that precedes cardiovascular diseases (CVDs) such as atherosclerosis, myocardial infarction, and stroke. NOX5 is the last discovered member of the NOX family, studied in a lesser extent due to its absence in the rodent genome. Our objective was to describe the phenotypic alterations produced by an oxidative stress situation derived from NOX5 overexpression in an endothelial in vitro model. The in vitro model consists of the hCMEC/D3 cell line, derived from brain microvascular endothelium, infected with a recombinant NOX5-β adenovirus. After an initial proteomic analysis, three phenotypic alterations detected in silico were studied: cell proliferation and apoptosis, general and mitochondrial metabolism, and migration capacity. NOX5 infection of hCMEC/D3 generates a functional protein and an increase in ROS production. This model produced changes in the whole cell proteome. The in silico analysis together with in vitro validations demonstrated that NOX5 overexpression inhibits proliferation and promotes apoptosis, metabolic alterations and cell migration in hCMEC/D3 cells. NOX5 overexpression in endothelial cells leads to phenotypic changes that can lead to endothelial dysfunction, the onset of atherosclerosis, myocardial infarction, and stroke.
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title_short	NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)
url	https://doi.org/10.3390/antiox11112147 https://doaj.org/article/efab88561a404aac86710e087b10b99c https://www.mdpi.com/2076-3921/11/11/2147 https://doaj.org/toc/2076-3921
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up_date	2024-07-03T17:19:41.121Z
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This model produced changes in the whole cell proteome. The in silico analysis together with in vitro validations demonstrated that NOX5 overexpression inhibits proliferation and promotes apoptosis, metabolic alterations and cell migration in hCMEC/D3 cells. 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NADPH Oxidase 5 (NOX5) Overexpression Promotes Endothelial Dysfunction via Cell Apoptosis, Migration, and Metabolic Alterations in Human Brain Microvascular Endothelial Cells (hCMEC/D3)

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