Mechanism of progression of neointimal hyperplasia at the vasada anastomatic strictwe : a study in tenascin-C Deficient Mice

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A simple aortotomy model was constructed using mice. In the wild-type mice, neointimal hyperplasia was observed at the suture sites at days 14 and 28. Immunohistochemical staining showed the strong expression of tenascin-C in both the neoinitima and media around the suture line at day 14. At day 28, tenascin-C staining was detected in the neointima, but not in the media. In the tenascin-C-deficient mice, much less neointimal hyperplasia was seen compared to in the wild-type mice and the mean neointima/media area ratio decreased to 45.4% and 30.5% at days 14 and 28, respectively. Proliferating cell nuclear antigen indeces in the wild-type mice were two times higher than those in the tenascin-C-deficient mice at day 14. Less alcian blue-positive proteoglycans were deposited in the neointima of the tenascin-C-deficient mice than the wild-type mice. These results suggest that tenascin-C promotes neointimal cell migration and proliferation, and deposition of proteoglycans. The current study provide direct evidence that tenascin-C is a key molecule in neointimal hyperplasia in anastomotic stenosis, implying its role as a target molecule for the prevention of stenosis.