Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice

Abstract The mechanisms responsible for macrovascular complications in diabetes remain to be fully understood. Recent studies have identified impaired vascular repair as a possible cause of plaque vulnerability in diabetes. This notion is supported by observations of a reduced content of fibrous pro...

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Autores principales:	Sabrina Hsiung, Anki Knutsson, Jenifer Vallejo, Pontus Dunér, Suvi E. Heinonen, Ann-Cathrine Jönsson-Rylander, Eva Bengtsson, Jan Nilsson, Anna Hultgårdh-Nilsson
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/163c2877f16246048be5c26530369fdb
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spelling	oai:doaj.org-article:163c2877f16246048be5c26530369fdb2021-12-02T15:05:02ZHyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice10.1038/s41598-018-25942-32045-2322https://doaj.org/article/163c2877f16246048be5c26530369fdb2018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25942-3https://doaj.org/toc/2045-2322Abstract The mechanisms responsible for macrovascular complications in diabetes remain to be fully understood. Recent studies have identified impaired vascular repair as a possible cause of plaque vulnerability in diabetes. This notion is supported by observations of a reduced content of fibrous proteins and smooth muscle cell mitogens in carotid endarterectomy from diabetic patients along with findings of decreased circulating levels of endothelial progenitor cells. In the present study we used a diabetic mouse model to characterize how hyperglycemia affects arterial repair responses. We induced atherosclerotic plaque formation in ApoE-deficient (ApoE−/−) and heterozygous glucokinase knockout ApoE-deficient mice (ApoE−/− GK+/−) mice with a shear stress-modifying cast. There were no differences in cholesterol or triglyceride levels between the ApoE−/− and ApoE−/− GK+/− mice. Hyperglycemia did not affect the size of the formed atherosclerotic plaques, and no effects were seen on activation of cell proliferation, smooth muscle cell content or on the expression and localization of collagen, elastin and several other extracellular matrix proteins. The present study demonstrates that hyperglycemia per se has no significant effects on tissue repair processes in injured mouse carotid arteries, suggesting that other mechanisms are involved in diabetic plaque vulnerability.Sabrina HsiungAnki KnutssonJenifer VallejoPontus DunérSuvi E. HeinonenAnn-Cathrine Jönsson-RylanderEva BengtssonJan NilssonAnna Hultgårdh-NilssonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-11 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sabrina Hsiung Anki Knutsson Jenifer Vallejo Pontus Dunér Suvi E. Heinonen Ann-Cathrine Jönsson-Rylander Eva Bengtsson Jan Nilsson Anna Hultgårdh-Nilsson Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice
description	Abstract The mechanisms responsible for macrovascular complications in diabetes remain to be fully understood. Recent studies have identified impaired vascular repair as a possible cause of plaque vulnerability in diabetes. This notion is supported by observations of a reduced content of fibrous proteins and smooth muscle cell mitogens in carotid endarterectomy from diabetic patients along with findings of decreased circulating levels of endothelial progenitor cells. In the present study we used a diabetic mouse model to characterize how hyperglycemia affects arterial repair responses. We induced atherosclerotic plaque formation in ApoE-deficient (ApoE−/−) and heterozygous glucokinase knockout ApoE-deficient mice (ApoE−/− GK+/−) mice with a shear stress-modifying cast. There were no differences in cholesterol or triglyceride levels between the ApoE−/− and ApoE−/− GK+/− mice. Hyperglycemia did not affect the size of the formed atherosclerotic plaques, and no effects were seen on activation of cell proliferation, smooth muscle cell content or on the expression and localization of collagen, elastin and several other extracellular matrix proteins. The present study demonstrates that hyperglycemia per se has no significant effects on tissue repair processes in injured mouse carotid arteries, suggesting that other mechanisms are involved in diabetic plaque vulnerability.
format	article
author	Sabrina Hsiung Anki Knutsson Jenifer Vallejo Pontus Dunér Suvi E. Heinonen Ann-Cathrine Jönsson-Rylander Eva Bengtsson Jan Nilsson Anna Hultgårdh-Nilsson
author_facet	Sabrina Hsiung Anki Knutsson Jenifer Vallejo Pontus Dunér Suvi E. Heinonen Ann-Cathrine Jönsson-Rylander Eva Bengtsson Jan Nilsson Anna Hultgårdh-Nilsson
author_sort	Sabrina Hsiung
title	Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice
title_short	Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice
title_full	Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice
title_fullStr	Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice
title_full_unstemmed	Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice
title_sort	hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in apoe−/− mice
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/163c2877f16246048be5c26530369fdb
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Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE−/− mice

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