肝切除后肝窦内皮细胞（LSECs）增殖延迟是制约肝再生的瓶颈。最新研究提出，术后骨髓内皮祖细胞（BM SPCs）被募集到肝脏，是肝血窦重建的主要细胞，SDF-1、CXCR4是BM SPCs动员、募集的关键分子。血管损伤修复的研究提示，VEGF是调节SDF-1表达的上游分子。我们前期研究表明，血管内皮生长因子（VEGF）具有促进肝再生的作用。由此我们提出假设：术后肝再生过程中VEGF/SDF-1/CXCR4途径是募集BM SPCs重建肝血窦完成肝再生的必要分子机制。为此，在本项目中我们将通过体内外两方面研究，阐述BM SPCs存在VEGF受体通路，并通过调节SDF-1/CXCR4途径来动员、募集BM SPCs参与肝再生。本项目旨在阐明术后肝再生中VEGF/SDF-1/CXCR4途径的作用机制，为肝再生研究提供实验基础，为临床促肝再生治疗提供理论依据。

The delay of proliferation in liver sinusoidal endothelial cells (LSECs) after hepatectomy is a rate-limiting step during liver regeneration. However, emerging data suggest that bone marrow sinusoidal progenitor cells of LSECs (BM SPCs) recruited to the liver postoperatively are the major drivers in reconstruction of liver sinusoid. Stromal-cell-derived factor 1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) are the key molecules in BM SPCs mobilization and recruitment. The research results of angiogenesis and injury repair show that the vascular endothelial growth factor (VEGF) is the upstream molecular on regulating the expression of SDF-1. Our previous study demonstrated that VEGF is a vital factor for improving liver regeneration. Thus, we hypothesize that VEGF/SDF-1/CXCR4 is the essential molecular mechanism in the recruitment of BM SPCs for liver sinusoid reconstruction and liver regeneration. For this purpose, we will perform both in vitro and in vivo experiments to illustrate that BM SPCs are mobilized and recruited throuth SDF-1/CXCR4 pathway regulated by VEGF/receptors. The ultimate goals of this project are to elucidate the mechanism of VEGF/SDF-1/CXCR4 pathway in liver regeneration after hepatectomy, and to develop experimental foundation for liver regeneration study and theoretical basis for clinical administration.