机构：[1]Department of Neurosurgery, West China Medical School, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China四川大学华西医院[2]Department of Neurosurgery, The First People’s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan Province, China外科片神经外科云南省第一人民医院[3]Department of Otolaryngology & Head and Neck Surgery, The First People’s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan Province, China外科片耳鼻喉科云南省第一人民医院[4]State Key Laboratory of Biotherapy and Cancer Center, Research Unit of Gene and Immunotherapy, Chinese Academy of Medical Sciences, Collaborative Innovation Center of Biotherapy, West China Hospital, Chengdu, Sichuan Province, China四川大学华西医院[5]Department of Neurosurgery, NHC Key Laboratory of Nuclear Technology Medical Transformation (Mianyang Central Hospital),School of Medicine, University of Electronic Science and Technology of China, Mianyang, Sichuan Province, China[6]Department of Neurosurgery, Fifth People’s Hospital of Ningxia Hui Autonomous Region, Shizuishan, Ningxia Hui Autonomous Region, China
Neural stem cells (NSCs) have the potential for self-renewal and multidirectional differentiation, and their transplantation has achieved good efficacy in a variety of diseases. However, only 1%-10% of transplanted NSCs survive in the ischemic and hypoxic microenvironment of posthemorrhagic hydrocephalus. Sox2 is an important factor for NSCs to maintain proliferation. Therefore, Sox2-overexpressing NSCs (NSCSox2) may be more successful in improving neurological dysfunction after posthemorrhagic hydrocephalus. In this study, human NSCSox2 was transplanted into a posthemorrhagic hydrocephalus mouse model, and retinoic acid was administered to further promote NSC differentiation. The results showed that NSCSox2 attenuated the ventricular enlargement caused by posthemorrhagic hydrocephalus and improved neurological function. NSCSox2 also promoted nerve regeneration, inhibited neuroinflammation and promoted M2 polarization (anti-inflammatory phenotype), thereby reducing cerebrospinal fluid secretion in choroid plexus. These findings suggest that NSCSox2 rescued ventricular enlargement and neurological dysfunction induced by posthemorrhagic hydrocephalus through neural regeneration and modulation of inflammation.
基金：
National Natural Science Foundation of China [82473334, 82401629]; Major Scientific and Technological Achievements Transformation Project of Ningxia Hui Autonomous Region [2022CJE09013]; Mianyang Science and Technology Bureau (Mianyang Science and Technology Program) [2023ZYDF097]; NHC Key Laboratory of Nuclear Technology Medical Transformation (Mianyang Central Hospital) [2023HYX001]; Spinal Cord Diseases Clinical Medical Center of Yunnan Province [2024JSKFKT-16]; Natural Science Foundation of Sichuan Province [2024NSFSC1646]; China Postdoctoral Science Foundation [GZC20231811, 2024T170601, 2024M76228]
第一作者机构：[1]Department of Neurosurgery, West China Medical School, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China[2]Department of Neurosurgery, The First People’s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan Province, China
共同第一作者：
通讯作者：
通讯机构：[1]Department of Neurosurgery, West China Medical School, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China[5]Department of Neurosurgery, NHC Key Laboratory of Nuclear Technology Medical Transformation (Mianyang Central Hospital),School of Medicine, University of Electronic Science and Technology of China, Mianyang, Sichuan Province, China[6]Department of Neurosurgery, Fifth People’s Hospital of Ningxia Hui Autonomous Region, Shizuishan, Ningxia Hui Autonomous Region, China
推荐引用方式(GB/T 7714)：
Gao Baocheng,Wang Haoxiang,Hu Shuang,et al.Sox2-overexpressing neural stem cells alleviate ventricular enlargement and neurological dysfunction in posthemorrhagic hydrocephalus[J].NEURAL REGENERATION RESEARCH.2026,21(2):769-779.doi:10.4103/NRR.NRR-D-24-01491.
