Copyright © 2007, European Society of Cardiology
Tenascin-C synthesized in both donor grafts and recipients accelerates artery graft stenosis
aDepartment of Thoracic and Cardiovascular Surgery, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan
bDepartment of Pathology and Matrix Biology, Mie University Graduate School of Medicine, Tsu, Mie, Japan
cDepartment of Physiology, Mie University Graduate School of Medicine, Tsu, Mie, Japan
* Corresponding author. Tel.: +81 59 232 1111; fax: +81 59 231 2845. Email address: k-onoda{at}clin.medic.mie-u.ac.jp
Objective: Tenascin-C, an extracellular matrix glycoprotein, is thought to play an important role in neointimal hyperplasia of artery bypass grafts. In this study, the direct contribution of tenascin-C to neointimal hyperplasia of free artery grafts and the origin of tenascin-C-producing cells were examined using tenascin-C transgenic mice.
Methods and results: Abdominal aorta-to-carotid artery interposition grafting was performed in mice. When grafts from wild-type mice were transplanted to wild-type, neointimal hyperplasia was observed in the grafts at days 14 and 28. Immunohistochemical staining showed strong expression of tenascin-C in the media and neointima of the grafts. Much less neointimal hyperplasia was seen when grafts from tenascin-C-deficient mice were transplanted to tenascin-C-deficient mice. In tenascin-C-deficient grafts transplanted to wild-type mice, tenascin-C deposition was observed only in the neointima. In the reverse combination, deposition was seen in the media and neointima. The source of the tenascin-C-producing cells was analyzed using heterozygous mice that identically express both tenascin-C and LacZ. While LacZ-positive cells were seen only in the neointima of artery grafts from wild-type transplanted to mutant mice, positive cells were detected in both the neointima and media in grafts from mutant to wild-type mice.
Conclusions: We presented direct evidence that tenascin-C is a crucial molecule in neointimal hyperplasia in free artery grafts, and that tenascin-C-producing cells are derived from both donor grafts and recipients.
KEYWORDS Cardiovascular surgery; Coronary disease; Remodeling; Transgenic animal models; Extracellular matrix
Time for primary review 45 days
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