Bone marrow stromal cells promote neuromotor functional recovery, via upregulation of neurotrophic factors and synapse proteins following traumatic brain injury in rats
- Yan Feng
- Yaru Ju
- Jianzhong Cui
- Liqun Wang
Affiliations: Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, Department of Obstetrics, The Fourth Hospital of Shijiazhuang, Shijiazhuang, Hebei 050011, P.R. China, Department of Neurosurgery, Tangshan Workers' Hospital, Tangshan, Hebei 063000, P.R. China
- Published online on: May 25, 2017 https://doi.org/10.3892/mmr.2017.6619
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It has previously been demonstrated that bone marrow stromal cells (BMSCs) exhibit great therapeutic potential in neuronal injuries; however, there is limited understanding of the precise underlying mechanisms that contribute to functional improvement following brain injury. The aim of the present study was to assess the effect of BMSC treatment on traumatic brain injury (TBI) in rats, and investigate if they migrate to injured areas and promote neuromotor functional recovery via upregulation of neurotrophic factors and synaptic proteins. BMSCs were cultured in vitro from female Sprague Dawley (SD) rat bone marrow and were subsequently infused into male adult SD rats via the tail vein, following induction of TBI. The results demonstrated that treatment with BMSCs significantly reduced TBI‑induced neuromotor impairment and neuronal loss, as assessed by rota rod testing, western blot analysis, modified neurological severity score and immunohistochemistry. The distribution of transplanted BMSCs was tracked by monitoring the expression of sex determining region Y (SRY) in rats. The number of cells double‑positive for SRY/neuronal nuclear antigen or SRY/glial fibrillary acidic protein was increased in the BMSC group, which demonstrated that BMSCs migrated to injured areas and differentiated into neurons and astrocytes, following TBI. Furthermore, administration of BMSCs increased expression of vascular endothelial growth factor and brain derived neurotrophic factor. Protein expression levels of synaptophysin were downregulated following TBI and this was reversed in part by treatment with BMSCs. These findings uncovered some underlying mechanisms of action of BMSCs, and may lead to their potential use as a future effective therapeutic agent for the treatment of TBI.