缺血性脑卒中再灌注（CIS/R）继发脑水肿损伤，是脑卒中患者致死致残主要原因，无有效治疗手段。转录因子MRTF-A可抑制缺氧缺血介导的神经元凋亡缓解CIS/R损伤，但具体机制不明。已知，精子相关抗原6（Spag6）缺失可致运动纤毛功能缺陷引发脑水肿。CIS/R过程中，定位于室管膜细胞和运动纤毛的MRTF-A、Spag6表达水平与运动纤毛结构紊乱程度呈正相关，且Spag6启动子上含MRTF-A结合位点（CarG盒）。提示MRTF-A可能是调节运动纤毛结构功能的重要因子，其可通过调控靶基因Spag6转录表达缓解CIS/R引发的脑水肿。因此，本研究以CIS/R为研究对象，采用慢病毒感染、电镜、EMSA等技术，在整体动物和细胞水平系统研究MRTF-A对Spag6的转录调控作用，及其在CIS/R过程中对室管膜细胞上运动纤毛结构功能的影响。课题的实施可望为CIS/R损伤的防治提供新思路和作用新靶点。

Cerebral ischemic stroke-reperfusion (CIS/R) following hydrocephalus is the principal cause of death and disability in patients with stroke that is no effective treatment. The transcription factor MRTF-A can restrain neuron apoptosis induced by hypoxia/ischemia, however the molecular mechanism remains unclear. The deficiency of sperm-associated antigen 6 (Spag6) leads to defect of structure and function of the motile cilia with hydrocephalus in mice. In the process of CIS/R, the expression of both MRTF-A and Spag6, which are located in the ependymal cells and motile cilia, is consistent with the structure disorder of motile cilia. In silico analysis shows a putative MRTF-A binding site (CarG box) in the Spag6 promoter region. It is suggested that MRTF-A may be an important factor for regulating the structure and function of motile cilia, which alleviates CIS/R-induced hydrocephalus by activating expression of Spag6. Thus, the purpose of this project is to study the role of MRTF-A on transcriptional regulation of Spag6 and its effect on the structure and function of motile cilia on ependymal cells during CIS/R in vitro and in vivo by comprehensive techniques, such as lentivirus infection, TEM, EMSA. This study will provide new theory basis for the prevention and treatment of CIS/R injury.