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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Main Authors: Naoya Hashikawa, Masanobu Ido, Yuna Morita, Narumi Hashikawa-Hobara
Format: Article
Language:English
Published: Nature Portfolio 2021-03-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-021-86601-8
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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
collection DOAJ
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.
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spelling doaj.art-cda20dfeb40b46dca7c40713396892e42022-12-21T21:20:53ZengNature PortfolioScientific Reports2045-23222021-03-0111111310.1038/s41598-021-86601-8Effects from the induction of heat shock proteins in a murine model due to progression of aortic atherosclerosisNaoya Hashikawa0Masanobu Ido1Yuna Morita2Narumi Hashikawa-Hobara3Department of Life Science, Okayama University of ScienceDepartment of Life Science, Okayama University of ScienceDepartment of Life Science, Okayama University of ScienceDepartment of Life Science, Okayama University of ScienceAbstract 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.https://doi.org/10.1038/s41598-021-86601-8
spellingShingle 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
Scientific Reports
title 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_short 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
url https://doi.org/10.1038/s41598-021-86601-8
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