心脏干细胞（CSC）通过旁分泌作用促进梗死后心肌修复，但CSC归巢至梗死心肌区域数量少，改善心脏功能有限。已证实心肌梗死区“边缘”心肌表达的腱生蛋白C通过其活性配体Toll样受体-4（TLR-4），促进多种细胞均有迁移、增殖及分化表达调节。CSC、心脏血管及内皮均表达TLR-4，我们的前期研究发现心肌梗死后患者血清Tenascin-C升高且Tenascin-C可以促进体外间充质干细胞迁移，但Tenascin-C是否作用于CSC及其表达的TLR4，并对CSC移植产生影响，目前尚不清楚。本研究拟获取TLR4-/、Tenascin-C-/-及野生型小鼠CSC；观察Tenascin-C对CSC的增殖、分化与迁移的影响；在体观察CSC移植到上述心肌梗死小鼠体内后，CSC归巢、增殖、分化及心脏功能的变化与Tenascin-C/TLR-4的关系，从而为提高CSC移植治疗心肌梗死疗效提供新的理轮依据。

Evidence suggests that cardiac stem cells (CSC) enhance heart function after acute myocardial infarction (AMI) via paracrine effects. The effects on heart function recovery are limited because a rare of population cells could be homing in infracted myocardium. It was showed that tenascin-C was expressed by myocardium in border zone during the acute stage after myocardial infarction and regulated several cellular functions associated with cell migration, proliferation and differentiation. Tenascin-C is also an endogenous activator of Toll-like receptor 4 (TLR-4). However, it is not clear whether tenascin-C regulates CSC by activating TLR-4. In our previous study, we have demonstrated that serum TN-C level increased in AMI patients. In addition, TN-C enhances MSCs migration in vitro. However, it is still unclear if the effects of TN-C on CSC via its TLR-4 after CSC transplantation in AMI therapy. Thus, in present study, CSC is isolated from TLR-4 knockout mice, Tenascin-C knockout mice and wild mice. After cultured with tenascin-C, the effects on CSC migration, proliferation and differentiation are explored in vitro. Furthermore, CSC is implanted into mice post-infarction. The effects of tenascin-C on heart function, CSC migration, proliferation and differentiation are investigated in vivo. It would provide new theoretical basis on stem cell therapy after myocardial infarction.