脑中风是成年人致残的首要原因，中风后神经功能的恢复是临床上迫切需要解决的问题。以少突胶质细胞（OLs）死亡和脱髓鞘为主要表现的白质完整性缺失及血脑屏障（BBB）破坏是神经功能损伤的重要病理基础。脑内OLs前体细胞即NG2细胞的增殖及分化出现障碍导致卒中后只有部分神经功能恢复。我们前期结果表明，中风后梗死区周边NG2增殖并伴有胶质细胞生长因子（GGF2）的增加；给予GGF2可促进NG2细胞增殖和分化并伴有miR-17~92/Pdlim5/ID2变化。基于GGF2在神经功能恢复及ID2在NG2细胞分化中的重要作用，我们提出假设：GGF2与NG2细胞上受体结合，通过miR-17~92/pdlim5/ID2促进其增殖和分化、修复白质及BBB、改善神经功能。本项目将在动物、细胞和分子水平研究GGF2促进NG2细胞增殖分化、改善卒中后神经功能恢复的作用及机制，从而为卒中后神经功能恢复提供新策略和靶点。

Stroke is the leading cause of adult disability. It is urgent to find a strategy to promote functional recovery after stroke in clinic. Disruption of white matter integrity, which is characterized by death of oligodendrocytes (OLs) and loss of myelin, and disruption of blood brain barrier (BBB) are the pathological base of disability of neural function. Disability of proliferation and differentiation of oligodendrocyte precursor cell (NG2 cell) are the main cause of limited functional recovery after stroke. Our preliminary data showed that there is a increase of NG2 cell accompanied by increase of glial growth factor (GGF2). GGF2 administration promotes proliferation and differentiation of NG2 cell accompanied by changes of miR-17~92/Pdlim5/ID2. Based on the important roles of GGF2 in functional recovery and ID2 in proliferation and differentiation of NG2 cell, we propose that after binding with receptor on the surface of NG2 cell, GGF2 could promote NG2 cell proliferation and differentiation by affecting miR-17~92/Pdlim5/ID2, repair the integrity of BBB and white matter, improve the neural function. In this study, using in vivo and in vitro ischemia stroke model, we will investigate the effect and mechanism of GGF2 treatment on NG2 cell proliferation, differentiation as well as functional recovery after stroke. Our aim is to provide new strategy to increase functional recovery after stroke.