脑损伤后干细胞移植进行神经修复所面临最大问题是移植细胞存活及增殖。我们首次发现炎症激活的星胶细胞（LPS-星胶细胞）及其释放的外泌体可促进脐带间充质干细胞（ucMSCs）增殖，但具体机制不明。我们前期研究通过测序筛选出LPS-星胶细胞中IGF-1及增殖ucMSCs中PBK这两个潜在靶点分子；并发现星胶细胞释放外泌体中携带IGF-1、增殖ucMSCs中存在PI3K磷酸化。由此我们提出“星胶细胞炎症激活后通过含有IGF-1外泌体调控ucMSCs中PBK及PI3K-AKT通路影响ucMSCs增殖”的假说。本课题拟首先阐明星胶细胞在炎症活化后IGF-1表达及外泌体释放变化的分子机制；分析外泌体中IGF-1如何经转录调控因子E2F1影响ucMSCs中PBK表达、调控PI3K-AKT通路；并研究增殖ucMSCs对LPS-星胶细胞的反馈，为脑损伤后开展ucMSCs/LPS-星胶细胞联合移植提供研究基础。

The major problem of neurogensis by stem cells transplantation after TBI is the survival and proliferation of transplanted cells. In our previous study, we first found that LPS activated Astrocytes (LPS-Astrocytes) or Exosome from these Astrocytes (Astrocytes-Exosome) could promote ucMSCs proliferation in vitro, however the mechanism remains uncovered. Through transcriptome sequencing, our research group have selected out IGF-1 in LPS-Astrocytes and PBK in proliferation ucMSCs as molecular targets. Meanwhile, we have demonstrated Astrocytes-Exosome contains IGF-1 and PI3K/AKT signaling was phosphyrylation activited in proliferation ucMSCs. Therefor, we propose that LPS-Astrocytes regulate PBK expression in ucMSCs through its Exosome containing IGF-1, then impact ucMSCs proliferation by PI3K/AKT signaling pathway. In this research, we intend to entirely investigate the interactions between LPS-Astrocytes and ucMSCs and the mechanism of LPS-Astrocytes or Exosome promoting ucMSCs proliferation from the perspective of “intercellular Cross-Talk”, explore the reason for IGF-1 change in Astrocytes after LPS stimulation, analyze the mechanism of Astrocytes-Exosome regulates PBK expression in ucMSCs, and clarify the whole signaling pathway under ucMSCs proliferation induced by LPS-Astrocytes. The results in this study will provide research foundation for LPS-Astrocytes/ucMSCs double cell transplantation after TBI.