The effects of BMSCs transplantation on autophagy by CX43 in the hippocampus following traumatic brain injury in rats

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• 作者：Liqian Sun (1)
  Junling Gao (2)
  Manman Zhao (2)
  Xiaobin Jing (3)
  Ying Cui (1)
  Xiaoyu Xu (1)
  Kaijie Wang (1)
  Wenqian Zhang (1)
  Jianzhong Cui (1)
  
• 关键词：Autophagy ; BMSCs ; CX43 ; Hippocampus ; Traumatic brain injury
• 刊名：Neurological Sciences
• 出版年：2014
• 出版时间：May 2014
• 年：2014
• 卷：35
• 期：5
• 页码：677-682
• 全文大小：
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• 作者单位：Liqian Sun (1)
  Junling Gao (2)
  Manman Zhao (2)
  Xiaobin Jing (3)
  Ying Cui (1)
  Xiaoyu Xu (1)
  Kaijie Wang (1)
  Wenqian Zhang (1)
  Jianzhong Cui (1)
  
  1. Department of Neurosurgery, Tangshan Gongren Hospital, No. 27 Wen Hua Road, Tangshan, 063000, People鈥檚 Republic of China
  2. School of Basic Medical Science, Hebei United University, No. 57 Jan She Road, Tangshan, 063000, People鈥檚 Republic of China
  3. Department of Ophthalmology, Tangshan Ophthalmology Hospital, No. 11 Bei Xin Road, Tangshan, 063000, People鈥檚 Republic of China
  
• ISSN：1590-3478

文摘

Traumatic brain injury (TBI) can initiate a series of complicated pathological events, and induce various types of neuronal cell death including autophagy and apoptosis. Currently, the treatment of TBI is one of the main challenges in neurobiology. In this regard, the administration of bone marrow stromal cells (BMSCs) represents a novel treatment modality for TBI. However, the protective mechanism of BMSCs was unknown in the TBI. The aim of the present study was to assess the effects of BMSCs on connexin 43(CX43) and autophagy in the hippocampus following TBI in rats. A rat model of TBI was created using a modified weight-drop device. Double-membrane structures in the process of autophagy formation were frequently observed in injured brain by electron microscopy. The levels of autophagic pathway associated proteins and CX43 were also detected by western blot analysis. Specifically, immunoblotting results showed that BMSCs treatment after TBI could down-regulate light chain 3 (LC3), Beclin-1 and CX43 expression in the hippocampus. Taken together, our results demonstrated that BMSCs were able to significantly suppress TBI-induced autophagy activity, and the potential mechanism by regulating CX43 levels.