Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE-/-mice
Hsiung, Sabrina LU ; Knutsson, Anki LU ; Vallejo, Jenifer LU ; Dunér, Pontus LU ; Heinonen, Suvi E. ; Jönsson-Rylander, Ann Cathrine ; Bengtsson, Eva LU
; Nilsson, Jan
LU
and Hultgårdh-Nilsson, Anna
LU
(2018)
In Scientific Reports
8(1).
- 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... (More)
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-/-A nd 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.
(Less)
- author
- Hsiung, Sabrina
LU
; Knutsson, Anki
LU
; Vallejo, Jenifer
LU
; Dunér, Pontus
LU
; Heinonen, Suvi E.
; Jönsson-Rylander, Ann Cathrine
; Bengtsson, Eva
LU
; Nilsson, Jan
LU
and Hultgårdh-Nilsson, Anna
LU
- organization
- publishing date
- 2018-12-01
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 8
- issue
- 1
- article number
- 7530
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:85046996712
- pmid:29760458
- ISSN
- 2045-2322
- DOI
- 10.1038/s41598-018-25942-3
- language
- English
- LU publication?
- yes
- id
- 6a4d259d-4647-488e-af93-9efe0fdbf30d
- date added to LUP
- 2018-05-28 09:46:03
- date last changed
- 2024-01-14 20:57:54
@article{6a4d259d-4647-488e-af93-9efe0fdbf30d,
abstract = {{<p>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-/-A nd 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.</p>}},
author = {{Hsiung, Sabrina and Knutsson, Anki and Vallejo, Jenifer and Dunér, Pontus and Heinonen, Suvi E. and Jönsson-Rylander, Ann Cathrine and Bengtsson, Eva and Nilsson, Jan and Hultgårdh-Nilsson, Anna}},
issn = {{2045-2322}},
language = {{eng}},
month = {{12}},
number = {{1}},
publisher = {{Nature Publishing Group}},
series = {{Scientific Reports}},
title = {{Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE-/-mice}},
url = {{http://dx.doi.org/10.1038/s41598-018-25942-3}},
doi = {{10.1038/s41598-018-25942-3}},
volume = {{8}},
year = {{2018}},
}