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Updated: Feb 25, 2026
Mouse Models for Graft Arteriosclerosis
Published on: May 14, 2013
Uremia does not affect neointima formation in mice
Annemarie Aarup1, Carsten H Nielsen2, Line S Bisgaard1
1Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Insights
Uremia, a complication of chronic kidney disease, did not accelerate atherosclerosis development in mouse carotid arteries after vascular injury. This study found no potentiation of neointima formation or changes in smooth muscle cell markers due to uremia.
Area of Science:
- Cardiovascular Science
- Nephrology
- Vascular Biology
Background:
- Atherosclerotic cardiovascular disease is a significant complication of chronic kidney disease (CKD).
- CKD-induced uremia alters smooth muscle cell (SMC) phenotype, potentially accelerating atherosclerosis.
- SMC phenotypic modulation is a critical factor in atherosclerotic lesion development.
Purpose of the Study:
- To investigate if uremia potentiates neointima formation following vascular injury in a mouse model.
- To determine the effect of uremia on SMC marker gene expression in injured arteries.
Main Methods:
- Induction of uremia via 5/6 nephrectomy in C57BL/6 wild-type and apolipoprotein E knockout mice.
- Carotid artery wire injury to induce neointima formation.
- Assessment of neointima formation, lesion composition (MRI, histology), and SMC marker gene expression.
Main Results:
- Wire injury induced neointima formation and SMC marker downregulation in both wild-type and knockout mice.
- Uremia did not potentiate neointima formation or alter intimal lesion composition.
- No significant effect of uremia on SMC marker gene expression in injured carotid arteries was observed.
Conclusions:
- Uremia does not accelerate neointima formation in response to carotid artery wire injury in mice.
- The findings suggest potential differences in uremia's effects on SMCs across various vascular beds.
- Further research is needed to understand the localized impact of uremia on vascular smooth muscle cells.
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.
