Chapter 33Tissue Remodeling in Vascular Wall in Kawasaki Disease-Related Vasculitis Model Mice
Yukako Yoshikane, Mitsuhisa Koga, Tamaki Cho, Kyoko Imanaka-Yoshida, Yumi Yamamoto, Junichi Hashimoto, Hiroki Aoki, Koichi Yoshimura, and Shinichi Hirose.
Author Information and AffiliationsPublished online: June 25, 2016.
Kawasaki disease is the most common acute systemic vasculitis of unknown etiology in children [1] and can cause inflammation of the coronary arteries leading to aneurysms. Tenascin-C, an extracellular matrix protein, and c-Jun N-terminal kinase (JNK), an intracellular signaling protein, are known to be associated with inflammation and tissue remodeling [2, 3]. The purpose of this study was to demonstrate tenascin-C and JNK might be involved in tissue remodeling in a Candida albicans-induced murine model of aneurysm.
Keywords:
Kawasaki disease, Tenascin-C, c-Jun N-terminal kinase, Aneurysm, RemodelingKawasaki disease is the most common acute systemic vasculitis of unknown etiology in children [1] and can cause inflammation of the coronary arteries leading to aneurysms. Tenascin-C, an extracellular matrix protein, and c-Jun N-terminal kinase (JNK), an intracellular signaling protein, are known to be associated with inflammation and tissue remodeling [2, 3]. The purpose of this study was to demonstrate tenascin-C and JNK might be involved in tissue remodeling in a Candida albicans-induced murine model of aneurysm.
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More than 80 % of the mice showed the macroscopic features of aneurysms in the aorta and/or iliac and coronary arteries.
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Marked inflammatory cell infiltration was observed in vascular wall and perivascular connective tissue, accompanied by fragmentation of elastic fibers.
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Expression of tenascin-C was highly observed in vascular wall, accompanied by active degradation of elastic fibers.
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Pharmacologic inhibition of JNK attenuated the aneurysm formation in the mice model.
In conclusion, these findings suggest that both tenascin-C and JNK are involved in abnormal tissue remodeling and inflammation in the Candida albicans-induced Kawasaki disease murine model of aneurysm and that JNK inhibition may represent a novel therapeutic target for preventing a Kawasaki disease-related aneurysm.
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