脊髓损伤（SCI）以其高致残率给社会和家庭带来了沉重负担，研究表明患者损伤处神经元凋亡与神经环路中断是脊髓损伤后结构重建和功能康复的一个难题。尽管骨髓间充质干细胞（BMSCs）移植治疗SCI取得了一定进展，但其确切机制尚未完全阐明。本研究首次发现BMSCs治疗SCI时和损伤神经元之间存在线粒体转移现象，并可改善损伤神经元的凋亡和运动功能。结合文献和预实验结果，我们发现CD157可能是BMSCs线粒体转移的一个关键调控因子。为此本研究拟观察过表达和抑制表达CD157的BMSCs线粒体释放变化，移植治疗体内、体外SCI模型，研究移植后不同时间段损伤神经元的凋亡、轴突再生、脊髓运动诱发电位和功能康复，以及CD157-cADPR-Ca2+信号通路的介导机制。研究结果有望阐明CD157-cADPR-Ca2+通路调控BMSCs释放线粒体的具体机制，为BMSCs治疗SCI提供新的理论基础和实验依据。

Spinal cord injury (SCI) caused heavy burden to the society and family due to its high disability rate. The studies show that neuronal apoptosis and nerve circuit interruption is a key problem of functional rehabilitation after injury. Although the transplantation of bone marrow mesenchymal stem cells (BMSCs) has made some progress in the treatment of SCI, the exact mechanism is still unclear. In the present study, we discovered for the first time that BMSCs could transfer mitochondria to the injured neurons, and it could improve the survival of injured neurons and functional rehabilitation. Combined with literature and our previous results, we found that CD157 might be a key factor in regulating mitochondrial transfer of BMSCs. The present study we will use adenovirus transfection technique, observe BMSCs with high and low expression of CD157 transplantation to spinal cord injury model in vitro and in vivo to study the mechanism of CD157-cyclic ADP ribose -Ca2+ signaling pathway in mitochondria transfer, neuronal survival, axonal regeneration, and motor function recovery. The results will for the first time clarify the mechanism of mitochondrial transfer of BMSCs and provide a new theoretical basis for the treatment of BMSCs on SCI.