Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis

Abstract Heat shock proteins (HSPs) are molecular chaperones that repair denatured proteins. The relationship between HSPs and various diseases has been extensively studied. However, the relationship between HSPs and atherosclerosis remains unclear. In this study, we induced the expression of HSPs a...

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Autores principales:	Naoya Hashikawa, Masanobu Ido, Yuna Morita, Narumi Hashikawa-Hobara
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/cda20dfeb40b46dca7c40713396892e4
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spelling	oai:doaj.org-article:cda20dfeb40b46dca7c40713396892e42021-12-02T14:25:16ZEffects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis10.1038/s41598-021-86601-82045-2322https://doaj.org/article/cda20dfeb40b46dca7c40713396892e42021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-86601-8https://doaj.org/toc/2045-2322Abstract Heat shock proteins (HSPs) are molecular chaperones that repair denatured proteins. The relationship between HSPs and various diseases has been extensively studied. However, the relationship between HSPs and atherosclerosis remains unclear. In this study, we induced the expression of HSPs and analyzed the effects on the development/progression of atherosclerosis in vivo. Remarkably, when HSPs were induced in apolipoprotein E deficient (ApoE−/−) mice prior to the formation of atheromas, the progression of atherosclerosis was inhibited; the short-term induction of HSPs significantly decreased the mRNA expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in the aorta. In contrast, the induction of HSPs after the formation of atheromas promoted the progression of atherosclerosis. In fact, the short-term induction of HSPs, after the formation of atheromas, significantly increased the mRNA expression of tumor necrosis factor-alpha, and interleukin 6 in the aorta. Of note, the induction of HSPs also promoted the formation of macrophage-derived foam cells. Overall, these results indicate that HSPs exerts different effects in the context of aortic atherosclerosis, depending on its degree of progression. Therefore, the induction and inhibition of HSPs should be considered for the prevention and treatment of atherosclerosis, respectively.Naoya HashikawaMasanobu IdoYuna MoritaNarumi Hashikawa-HobaraNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Naoya Hashikawa Masanobu Ido Yuna Morita Narumi Hashikawa-Hobara Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
description	Abstract Heat shock proteins (HSPs) are molecular chaperones that repair denatured proteins. The relationship between HSPs and various diseases has been extensively studied. However, the relationship between HSPs and atherosclerosis remains unclear. In this study, we induced the expression of HSPs and analyzed the effects on the development/progression of atherosclerosis in vivo. Remarkably, when HSPs were induced in apolipoprotein E deficient (ApoE−/−) mice prior to the formation of atheromas, the progression of atherosclerosis was inhibited; the short-term induction of HSPs significantly decreased the mRNA expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in the aorta. In contrast, the induction of HSPs after the formation of atheromas promoted the progression of atherosclerosis. In fact, the short-term induction of HSPs, after the formation of atheromas, significantly increased the mRNA expression of tumor necrosis factor-alpha, and interleukin 6 in the aorta. Of note, the induction of HSPs also promoted the formation of macrophage-derived foam cells. Overall, these results indicate that HSPs exerts different effects in the context of aortic atherosclerosis, depending on its degree of progression. Therefore, the induction and inhibition of HSPs should be considered for the prevention and treatment of atherosclerosis, respectively.
format	article
author	Naoya Hashikawa Masanobu Ido Yuna Morita Narumi Hashikawa-Hobara
author_facet	Naoya Hashikawa Masanobu Ido Yuna Morita Narumi Hashikawa-Hobara
author_sort	Naoya Hashikawa
title	Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
title_short	Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
title_full	Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
title_fullStr	Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
title_full_unstemmed	Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
title_sort	effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/cda20dfeb40b46dca7c40713396892e4
work_keys_str_mv	AT naoyahashikawa effectsfromtheinductionofheatshockproteinsinamurinemodelduetoprogressionofaorticatherosclerosis AT masanobuido effectsfromtheinductionofheatshockproteinsinamurinemodelduetoprogressionofaorticatherosclerosis AT yunamorita effectsfromtheinductionofheatshockproteinsinamurinemodelduetoprogressionofaorticatherosclerosis AT narumihashikawahobara effectsfromtheinductionofheatshockproteinsinamurinemodelduetoprogressionofaorticatherosclerosis
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Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosis

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