You-Cui Wang1, Qing-Jie Xia2, Ying-Chun Ba3, Ting-Yong Wang3, Na LiN3, Yu Zou2, Fei-Fei Shang2, Xin-Fu Zhou4, Ting-Hua Wang5, Xue-Mei Fu6, Jian-Guo Qi7. 1. Department of Histology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China. 2. Institute of Neurobiological Disease, Translational Neuroscience Center and the State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. 3. Institute of Neuroscience, Kunming Medical University, Kunming, China. 4. School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia. 5. Department of Histology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China; Institute of Neurobiological Disease, Translational Neuroscience Center and the State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China; Institute of Neuroscience, Kunming Medical University, Kunming, China. 6. Shenzhen Children's Hospital, Shenzhen, Guangdong, China. Electronic address: fxm2j2004@163.com. 7. Department of Histology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China. Electronic address: jgqi@scu.edu.cn.
Abstract
BACKGROUND AIMS: The neuroprotective effects of olfactory ensheathing cells (OECs) after transplantation have largely been known in the injured nervous system. However, the underlying mechanisms still must be further elucidated. We explored the effects of OEC transplantation on the recovery of neurophysiologic function and the related anti-apoptosis mechanism in acute traumatic brain injury. METHODS: The OECs from neonatal Sprague-Dawley rats were isolated, identified and labeled and then were immediately transplanted into the regions surrounding the injured brain site that is resulted from free-weight drop injury. RESULTS: Nerve growth factor and it's recepor, p75 was expressed in cultured OECs. Transplanted OECs survived, migrated around the injury site and significantly improved the neurological severe scores compared with the control group (P < 0.05). OEC transplantation significantly increased the number of GAP-43-immunopositive fibers and synaptophysin-positive vesicles (P < 0.05) but significantly decreased the number of apoptotic cells (P < 0.05). On the molecular level, the expression of Bad in the OEC transplantation group was significantly downregulated (P < 0.05). CONCLUSIONS: OEC transplantation could effectively improve neurological deficits in TBI rats; the underlying mechanism may be related with their effects on neuroprotection and regeneration induction, which is associated with the downregulation of the apoptotic molecule Bad.
BACKGROUND AIMS: The neuroprotective effects of olfactory ensheathing cells (OECs) after transplantation have largely been known in the injured nervous system. However, the underlying mechanisms still must be further elucidated. We explored the effects of OEC transplantation on the recovery of neurophysiologic function and the related anti-apoptosis mechanism in acute traumatic brain injury. METHODS: The OECs from neonatal Sprague-Dawley rats were isolated, identified and labeled and then were immediately transplanted into the regions surrounding the injured brain site that is resulted from free-weight drop injury. RESULTS: Nerve growth factor and it's recepor, p75 was expressed in cultured OECs. Transplanted OECs survived, migrated around the injury site and significantly improved the neurological severe scores compared with the control group (P < 0.05). OEC transplantation significantly increased the number of GAP-43-immunopositive fibers and synaptophysin-positive vesicles (P < 0.05) but significantly decreased the number of apoptotic cells (P < 0.05). On the molecular level, the expression of Bad in the OEC transplantation group was significantly downregulated (P < 0.05). CONCLUSIONS: OEC transplantation could effectively improve neurological deficits in TBI rats; the underlying mechanism may be related with their effects on neuroprotection and regeneration induction, which is associated with the downregulation of the apoptotic molecule Bad.
Authors: Mei-Ling Luo; Lu Pan; Li Wang; Hai-Yan Wang; Sen Li; Zai-Yun Long; Lin Zeng; Yuan Liu Journal: Neurochem Res Date: 2019-11-07 Impact factor: 3.996