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

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Abstract

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.

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Abbreviations

CX43:

Connexin 43

BMSCs:

Bone marrow stromal cells

CNS:

Central nervous system

LC3:

Light chain 3

NeuN:

Neuronal nuclei

PBS:

Phosphate-buffered saline

TBI:

Traumatic brain injury

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Acknowledgments

The present study was supported by a grant from the Natural Science Foundation of Hebei Province (No. H2012401071).

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The authors declare that they have no conflict of interest.

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Correspondence to Liqian Sun.

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Sun, L., Gao, J., Zhao, M. et al. The effects of BMSCs transplantation on autophagy by CX43 in the hippocampus following traumatic brain injury in rats. Neurol Sci 35, 677–682 (2014). https://doi.org/10.1007/s10072-013-1575-6

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  • DOI: https://doi.org/10.1007/s10072-013-1575-6

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