| Research Abstract |
To clarify the roles and the expression regulation mechanism, we examined the localization of tenascin-C and its producing cells during myocardial tissue remodeling. Tenascin-C,which was not expressed in normal adult heart, was re-expressed by interstitial cells in myocardium of various experimental animal models, human autopsy or biopsy specimen. In case of acute myocardial infarction, tenascin-C appeared during acute phase at only the edge of residual myocardium.
Next, we analyzed the spatiotemporal distribution of tenascin-C and tenascin-X during the heart development of mouse embryos. Tenascin-C transiently appeared in (1) epithelializing and differentiating precardiac mesoderm (2) migrating endocardial cells into cardiac jelly, and (3) migrating proepicardial cells from transverse septum.
Tenascin-X was reciprocally expressed by epicardial cells migrating into myocardium after the expression of tenascin-X was downregulated. Tenascin-C null mice did not show any distinct phenotype. We have not find any indications that tenascin-X compensated tenascin-C.Furthermore, we examined factors which stimulate cardiac fibroblasts to synthesis tenascin-C in vitro. We have found that TGF-beta1, bFGF,angiotensin II,mechanical stretch, low pH,hypoxia induce the expression of tenascin-C.
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