Uremia does not affect neointima formation in mice
Abstract Atherosclerotic cardiovascular disease is a major complication of chronic kidney disease (CKD). CKD leads to uremia, which modulates the phenotype of aortic smooth muscle cells (SMCs). Phenotypic modulation of SMCs plays a key role in accelerating atherosclerosis. We investigated the hypoth...
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Nature Portfolio
2017-07-01
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Series: | Scientific Reports |
Online Access: | https://doi.org/10.1038/s41598-017-06816-6 |
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author | Annemarie Aarup Carsten H. Nielsen Line S. Bisgaard Ilze Bot Henrik H. El-Ali Andreas Kjaer Lars B. Nielsen Tanja X. Pedersen |
author_facet | Annemarie Aarup Carsten H. Nielsen Line S. Bisgaard Ilze Bot Henrik H. El-Ali Andreas Kjaer Lars B. Nielsen Tanja X. Pedersen |
author_sort | Annemarie Aarup |
collection | DOAJ |
description | Abstract Atherosclerotic cardiovascular disease is a major complication of chronic kidney disease (CKD). CKD leads to uremia, which modulates the phenotype of aortic smooth muscle cells (SMCs). Phenotypic modulation of SMCs plays a key role in accelerating atherosclerosis. We investigated the hypothesis that uremia potentiates neointima formation in response to vascular injury in mice. Carotid wire injury was performed on C57BL/6 wt and apolipoprotein E knockout (Apoe −/−) mice two weeks after induction of uremia by 5/6 nephrectomy. Wire injury led to neointima formation and downregulation of genes encoding classical SMC markers (i.e., myocardin, α-smooth muscle actin, SM22-alpha, and smooth muscle myosin heavy chain) in both wt and Apoe −/− mice. Contrary to our expectations, uremia did not potentiate neointima formation, nor did it affect intimal lesion composition as judged from magnetic resonance imaging and histological analyses. Also, there was no effect of uremia on SMC marker gene expression in the injured carotid arteries, suggesting that there may be different effects of uremia on SMCs in different vascular beds. In conclusion, uremia does not accelerate neointima formation in response to wire injury of the carotid artery in mice. |
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language | English |
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spelling | doaj.art-c01d0b83ed9c46878998b6f64f53187a2022-12-21T19:33:01ZengNature PortfolioScientific Reports2045-23222017-07-01711810.1038/s41598-017-06816-6Uremia does not affect neointima formation in miceAnnemarie Aarup0Carsten H. Nielsen1Line S. Bisgaard2Ilze Bot3Henrik H. El-Ali4Andreas Kjaer5Lars B. Nielsen6Tanja X. Pedersen7Department of Biomedical Sciences, University of CopenhagenDepartment of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Rigshospitalet, University of CopenhagenDepartment of Biomedical Sciences, University of CopenhagenDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden UniversityDepartment of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Rigshospitalet, University of CopenhagenDepartment of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Rigshospitalet, University of CopenhagenDepartment of Biomedical Sciences, University of CopenhagenDepartment of Biomedical Sciences, University of CopenhagenAbstract Atherosclerotic cardiovascular disease is a major complication of chronic kidney disease (CKD). CKD leads to uremia, which modulates the phenotype of aortic smooth muscle cells (SMCs). Phenotypic modulation of SMCs plays a key role in accelerating atherosclerosis. We investigated the hypothesis that uremia potentiates neointima formation in response to vascular injury in mice. Carotid wire injury was performed on C57BL/6 wt and apolipoprotein E knockout (Apoe −/−) mice two weeks after induction of uremia by 5/6 nephrectomy. Wire injury led to neointima formation and downregulation of genes encoding classical SMC markers (i.e., myocardin, α-smooth muscle actin, SM22-alpha, and smooth muscle myosin heavy chain) in both wt and Apoe −/− mice. Contrary to our expectations, uremia did not potentiate neointima formation, nor did it affect intimal lesion composition as judged from magnetic resonance imaging and histological analyses. Also, there was no effect of uremia on SMC marker gene expression in the injured carotid arteries, suggesting that there may be different effects of uremia on SMCs in different vascular beds. In conclusion, uremia does not accelerate neointima formation in response to wire injury of the carotid artery in mice.https://doi.org/10.1038/s41598-017-06816-6 |
spellingShingle | Annemarie Aarup Carsten H. Nielsen Line S. Bisgaard Ilze Bot Henrik H. El-Ali Andreas Kjaer Lars B. Nielsen Tanja X. Pedersen Uremia does not affect neointima formation in mice Scientific Reports |
title | Uremia does not affect neointima formation in mice |
title_full | Uremia does not affect neointima formation in mice |
title_fullStr | Uremia does not affect neointima formation in mice |
title_full_unstemmed | Uremia does not affect neointima formation in mice |
title_short | Uremia does not affect neointima formation in mice |
title_sort | uremia does not affect neointima formation in mice |
url | https://doi.org/10.1038/s41598-017-06816-6 |
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