Neural Stem Cells Transfected with Leukemia Inhibitory Factor Promote Neuroprotection in a Rat Model of Cerebral Ischemia.
10.1007/s12264-019-00405-5
- Author:
Lili TIAN
1
;
Wenli ZHU
1
;
Yuanchu LIU
2
;
Ye GONG
2
;
Aowei LV
1
;
Zhen WANG
2
;
Xiaoli DING
2
;
Shaowu LI
3
;
Ying FU
2
;
Yi LIN
4
;
Yaping YAN
5
Author Information
1. Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
2. Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, China.
3. Department of Function Neuroimaging, Neurosurgical Institute, Capital Medical University, Beijing, 100050, China.
4. Department of Neurology and Institute of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350000, China. linyi7811@163.com.
5. Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. yaping.yan@snnu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Cerebral ischemia;
Infarction volume;
Leukemia inhibitory factor;
Neural stem cells;
Neurological recovery
- From:
Neuroscience Bulletin
2019;35(5):901-908
- CountryChina
- Language:English
-
Abstract:
Leukemia inhibitory factor (LIF) contributes to the neuroprotection by neural stem cells (NSCs) after ischemic stroke. Our aim was to explore whether LIF-transfected NSCs (LIF-NSCs) can ameliorate brain injury and promote neuroprotection in a rat model of cerebral ischemia. To accomplish this goal, we transfected NSCs with a lentivirus carrying the LIF gene to stably overexpress LIF. The LIF-NSCs reduced caspase 3 activation under conditions of oxygen-glucose deprivation in vitro. Transient cerebral ischemia was induced in rats by 2 h of middle cerebral artery occlusion (MCAo), and LIF-NSCs were intravenously injected at 6 h post-ischemia. LIF-NSC treatment reduced the infarction volume and improved neurological recovery. Moreover, LIF-NSCs improved glial cell regeneration and ameliorated white matter injury in the MCAo rats. The NSCs acted as carriers and increased the expression of LIF in the lesions to protect against cerebral infarction, suggesting that LIF-NSCs could be a potential treatment for cerebral infarction.
