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Published on: May 14, 2013
Statin suppresses the development of excessive intimal proliferation in a Kawasaki disease mouse model
Yusuke Motoji1, Ryuji Fukazawa2, Ryosuke Matsui2
1Department of Cardiovascular Surgery, Kitasato University School of Medicine, Tokyo, Japan.
Insights
Statins significantly reduced neointimal hyperplasia in a mouse model of Kawasaki disease (KD). This suggests statins may effectively treat coronary artery lesions (CALs) by inhibiting vascular remodeling in KD patients.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- Kawasaki disease (KD) leads to vascular injury and coronary artery lesions (CALs) due to intimal proliferation.
- The mechanisms of vascular remodeling in KD and the role of statin treatment remain unclear.
Purpose of the Study:
- To investigate the effects of statins on vascular remodeling in a mouse model of KD.
- To explore the potential of statins in managing CALs associated with KD.
Main Methods:
- A mouse model of KD was established using Candida albicans water-soluble substance (CAWS) in apolipoprotein-E-deficient mice.
- Mice were treated with atorvastatin at different time points.
- Vascular remodeling was evaluated using Elastica van Gieson staining and immunostaining.
Main Results:
- Statins markedly suppressed neointimal hyperplasia induced by CAWS.
- CAWS-induced expression of TGFβ receptor II and MAC-2 around coronary arteries was reduced by statins.
- Statins demonstrated anti-inflammatory effects, inhibiting neointimal proliferation.
Conclusions:
- KD-like vasculitis promotes aneurysm formation and vascular stenosis.
- Statins may inhibit vascular remodeling by suppressing neointimal proliferation.
- Statin therapy could be beneficial for adult KD patients with CALs.
Abstract:
Kawasaki disease (KD) causes vascular injury and lifelong remodeling. Excessive intimal proliferation has been observed, resulting in coronary artery lesions (CALs). However, the mechanisms underlying vascular remodeling in CAL and statin treatment have not been comprehensively elucidated. This study aimed to investigate the effects of statins on vascular remodeling using a KD mouse model. Candida albicans water-soluble substance (CAWS) was intraperitoneally injected in 5-week-old male apolipoprotein-E-deficient mice. They were categorized as follows (n = 4): control, CAWS, CAWS+statin, and late-statin groups. The mice were euthanized at 6 or 10 weeks after injection. Statins (atorvastatin) were initiated after CAWS injection, except for the late-statin group, for which statins were internally administered 6 weeks after injection. Elastica van Gieson staining and immunostaining were performed for evaluation. Statins substantially suppressed the marked neointimal hyperplasia induced by CAWS. Additionally, CAWS induced TGFβ receptor II and MAC-2 expression around the coronary arteries, which was suppressed by the statins. KD-like vasculitis might promote the formation of aneurysm by destroying elastic laminae and inducing vascular stenosis by neointimal proliferation. The anti-inflammatory effects of statins might inhibit neointimal proliferation. Therefore, statin therapy might be effective in adult patients with KD with CAL by inhibiting vascular remodeling.
