A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

Abstract Our study tested the proposal that c-Myc activation in macrophages is differentially carried out dependent on the intracellular oxidative state of cells and potentially associated to the process of atherogenesis. Under our experimental conditions, the generation of reactive oxygen species c...

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Autores principales:	Victor García-González, Jaime Mas-Oliva
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7f1fe1f65f264017bc744ab675a95fa7
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spelling	oai:doaj.org-article:7f1fe1f65f264017bc744ab675a95fa72021-12-02T15:05:00ZA Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis10.1038/s41598-017-13880-52045-2322https://doaj.org/article/7f1fe1f65f264017bc744ab675a95fa72017-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-13880-5https://doaj.org/toc/2045-2322Abstract Our study tested the proposal that c-Myc activation in macrophages is differentially carried out dependent on the intracellular oxidative state of cells and potentially associated to the process of atherogenesis. Under our experimental conditions, the generation of reactive oxygen species carried out by the presence of oxidized low density lipoproteins (oxLDL) or Gram negative bacterial lipopolysaccharides (LPS) modifies the expression of cellular adhesion molecules such as c-Abl, calcium transport proteins such as the plasma membrane Ca2+-ATPase (PMCA), CD47, procaspase-7, CASP7, CHOP, transcriptional activators such as c-Jun and c-Myc and molecules that participate in the process of endocytosis like α- and β-adaptin. We present the first evidence showing that a state of oxidative stress alters c-Myc-dependent activity pathways in macrophages through binding to molecules such as β-adaptin promoting the reversible formation of a complex that presents the ability to regulate the development of the cell cycle. We propose that the subtle regulation carried out through the formation of this c-Myc/β-adaptin complex when cells change from a normal physiological condition to a state of oxidative stress, represents a defense mechanism against the deleterious effects caused by the loss of cell homeostasis.Victor García-GonzálezJaime Mas-OlivaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Victor García-González Jaime Mas-Oliva A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis
description	Abstract Our study tested the proposal that c-Myc activation in macrophages is differentially carried out dependent on the intracellular oxidative state of cells and potentially associated to the process of atherogenesis. Under our experimental conditions, the generation of reactive oxygen species carried out by the presence of oxidized low density lipoproteins (oxLDL) or Gram negative bacterial lipopolysaccharides (LPS) modifies the expression of cellular adhesion molecules such as c-Abl, calcium transport proteins such as the plasma membrane Ca2+-ATPase (PMCA), CD47, procaspase-7, CASP7, CHOP, transcriptional activators such as c-Jun and c-Myc and molecules that participate in the process of endocytosis like α- and β-adaptin. We present the first evidence showing that a state of oxidative stress alters c-Myc-dependent activity pathways in macrophages through binding to molecules such as β-adaptin promoting the reversible formation of a complex that presents the ability to regulate the development of the cell cycle. We propose that the subtle regulation carried out through the formation of this c-Myc/β-adaptin complex when cells change from a normal physiological condition to a state of oxidative stress, represents a defense mechanism against the deleterious effects caused by the loss of cell homeostasis.
format	article
author	Victor García-González Jaime Mas-Oliva
author_facet	Victor García-González Jaime Mas-Oliva
author_sort	Victor García-González
title	A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis
title_short	A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis
title_full	A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis
title_fullStr	A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis
title_full_unstemmed	A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis
title_sort	novel β-adaptin/c-myc complex formation modulated by oxidative stress in the control of the cell cycle in macrophages and its implication in atherogenesis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/7f1fe1f65f264017bc744ab675a95fa7
work_keys_str_mv	AT victorgarciagonzalez anovelbadaptincmyccomplexformationmodulatedbyoxidativestressinthecontrolofthecellcycleinmacrophagesanditsimplicationinatherogenesis AT jaimemasoliva anovelbadaptincmyccomplexformationmodulatedbyoxidativestressinthecontrolofthecellcycleinmacrophagesanditsimplicationinatherogenesis AT victorgarciagonzalez novelbadaptincmyccomplexformationmodulatedbyoxidativestressinthecontrolofthecellcycleinmacrophagesanditsimplicationinatherogenesis AT jaimemasoliva novelbadaptincmyccomplexformationmodulatedbyoxidativestressinthecontrolofthecellcycleinmacrophagesanditsimplicationinatherogenesis
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A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

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