Wu Hongjie, Li Jing, Xu Dongxiao, Zhang Qiansheng, Cui Tao
Department of Neurosurgery The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Front Neurol. 2018 Jul 23;9:592. doi: 10.3389/fneur.2018.00592. eCollection 2018.
The aim of this study was to investigate the therapeutic effect of growth differentiation factor 5 (GDF-5) on traumatic brain injury (TBI) in mice. We utilized a controlled cortical impact to establish a mouse TBI model, and then stereotaxically administered 25 or 100 ng GDF-5 into the bilateral hippocampal dentate gyrus (DG) of each of the animals. Seven days after the injury, some of the animals were sacrificed for immunohistochemical and immunofluorescence examination of 5-bromo-2'-deoxyuridine (BrdU), Sox-2, doublecortin (DCX) and phosphorylated cAMP response element binding protein (p-CREB). Dendrite quantification was also performed using DCX positive cells. Activation of newborn neurons was assessed 35 days after the injury. The remaining animals were subjected to open field, Y maze and contextual fear conditioning tests 2 months after TBI. As a result, we found that post-injury stereotaxical administration of GDF-5 can improve neural stem cell proliferation and differentiation in the DG of the hippocampus, evidenced by the increase in BrdU, Sox-2, and DCX-labeled cells, as well as the improvement in dendrite arborization and newborn neuron activation in response to GDF-5 treatment. Mechanistically, these effects of GDF-5 may be mediated by the CREB pathway, manifested by the recovery of TBI-induced dephosphorylation of CREB upon GDF-5 administration. Behavioral tests further verified the effects of GDF-5 on improving cognitive and behavioral dysfunction after TBI. Collectively, these results reveal that direct injection of GDF-5 into the hippocampus can stimulate neurogenesis and improve functional recovery in a mouse TBI model, indicating the potential therapeutic effects of GDF-5 on TBI.
本研究旨在探讨生长分化因子5(GDF-5)对小鼠创伤性脑损伤(TBI)的治疗作用。我们利用控制性皮质撞击建立小鼠TBI模型,然后通过立体定向向每只动物的双侧海马齿状回(DG)注射25或100 ng GDF-5。损伤后7天,处死部分动物,进行5-溴-2'-脱氧尿苷(BrdU)、Sox-2、双皮质素(DCX)和磷酸化环磷酸腺苷反应元件结合蛋白(p-CREB)的免疫组织化学和免疫荧光检测。还使用DCX阳性细胞进行树突定量分析。在损伤后35天评估新生神经元的激活情况。其余动物在TBI后2个月进行旷场、Y迷宫和情境恐惧条件测试。结果发现,损伤后立体定向注射GDF-5可改善海马DG区神经干细胞的增殖和分化,表现为BrdU、Sox-2和DCX标记细胞增多,以及GDF-5治疗后树突分支和新生神经元激活得到改善。从机制上讲,GDF-5的这些作用可能由CREB途径介导,表现为给予GDF-5后TBI诱导的CREB去磷酸化得以恢复。行为测试进一步证实了GDF-5对改善TBI后认知和行为功能障碍的作用。总的来说,这些结果表明,在小鼠TBI模型中,向海马直接注射GDF-5可刺激神经发生并改善功能恢复,提示GDF-5对TBI具有潜在治疗作用。