| First Author | Yamamoto K | Year | 2005 |
| Journal | Cardiovasc Res | Volume | 65 |
| Issue | 3 | Pages | 737-42 |
| PubMed ID | 15664401 | Mgi Jnum | J:162742 |
| Mgi Id | MGI:4819696 | Doi | 10.1016/j.cardiores.2004.10.034 |
| Citation | Yamamoto K, et al. (2005) Tenascin-C is an essential factor for neointimal hyperplasia after aortotomy in mice. Cardiovasc Res 65(3):737-42 |
| abstractText | OBJECTIVE: Neointimal hyperplasia at the arterial anastomotic site is a critical problem during cardiovascular surgery. It has been suggested that tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, might play an important role in neointimal hyperplasia. In this study, the direct contribution of tenascin-C to neointimal hyperplasia after aortotomy was examined using tenascin-C-deficient (TNKO) mice. METHODS AND RESULTS: A simple aortotomy model was constructed in mice. In wild-type (WT) mice, neointimal hyperplasia was observed at the suture sites at days 14 and 28. Immunohistochemical staining showed strong expression of tenascin-C in both neointima and media around the suture line at day 14. At day 28, tenascin-C staining was detected in neointima, but not in media. In tenascin-C-deficient mice, much less neointimal hyperplasia was seen compared to that in wild-type mice, and the mean neointima/media area ratio decreased to 52.8% and 34.3% at days 14 and 28, respectively. The proliferating cell nuclear antigen indices in wild-type mice were twice those in tenascin-C-deficient mice at day 14. There were fewer Alcian blue-positive proteoglycans deposited in the neointima of tenascin-C-deficient mice than in wild-type mice. These results suggest that tenascin-C promotes neointimal cell migration and proliferation, and the deposition of proteoglycans. CONCLUSIONS: We have presented direct evidence that tenascin-C is a crucial molecule in neointimal hyperplasia at anastomotic sites. |
