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首页> 美国卫生研究院文献>Experimental Neurobiology >Absence of Glia Maturation Factor Protects from Axonal Injury and Motor Behavioral Impairments after Traumatic Brain Injury
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Absence of Glia Maturation Factor Protects from Axonal Injury and Motor Behavioral Impairments after Traumatic Brain Injury

机译：胶质细胞成熟因子的缺乏防止轴突。损伤和运动行为障碍后创伤性脑损伤

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Traumatic brain injury (TBI) causes disability and death, accelerating the progression towards Alzheimer’s disease and Parkinson’s disease (PD). TBI causes serious motor and cognitive impairments, as seen in PD that arise during the period of the initial insult. However, this has been understudied relative to TBI induced neuroinflammation, motor and cognitive decline that progress towards PD. Neuronal ubiquitin-C-terminal hydrolase-L1 (UCHL1) is a thiol protease that breaks down ubiquitinated proteins and its level represents the severity of TBI. Previously, we demonstrated the molecular action of glia maturation factor (GMF); a proinflammatory protein in mediating neuroinflammation and neuronal loss. Here, we show that the weight drop method induced TBI neuropathology using behavioral tests, western blotting, and immunofluorescence techniques on sections from wild type (WT) and GMF-deficient (GMF-KO) mice. Results reveal a significant improvement in substantia nigral tyrosine hydroxylase and dopamine transporter expression with motor behavioral performance in GMF-KO mice following TBI. In addition, a significant reduction in neuroinflammation was manifested, as shown by activation of nuclear factor-kB, reduced levels of inducible nitric oxide synthase, and cyclooxygenase-2 expressions. Likewise, neurotrophins including brain-derived neurotrophic factor and glial-derived neurotrophic factor were significantly improved in GMF-KO mice than WT 72 h post-TBI. Consistently, we found that TBI enhances GFAP and UCHL-1 expression and reduces the number of dopaminergic TH-positive neurons in WT compared to GMF-KO mice 72 h post-TBI. Interestingly, we observed a reduction of TH-positive tanycytes in the median eminence of WT than GMF-KO mice. Overall, we found that absence of GMF significantly reversed these neuropathological events and improved behavioral outcome. This study provides evidence that PD-associated pathology progression can be initiated upon induction of TBI.
机译：颅脑外伤（TBI）会导致残疾和死亡，并加速阿尔茨海默氏病和帕金森氏病（PD）的发展。 TBI会导致严重的运动和认知障碍，如PD在初始侮辱期间出现的那样。但是，相对于TBI诱发的PD引起的神经炎症，运动和认知功能下降，这方面的研究还不足。神经元泛素C末端水解酶L1（UCHL1）是一种硫醇蛋白酶，可分解泛素化的蛋白质，其水平代表TBI的严重程度。先前，我们证明了神经胶质成熟因子（GMF）的分子作用;介导神经炎症和神经元丢失的促炎蛋白。在这里，我们显示了从行为学，蛋白质印迹和免疫荧光技术对野生型（WT）和GMF缺陷型（GMF-KO）小鼠的切片使用行为测试，免疫印迹和免疫荧光技术，体重减轻方法诱导的TBI神经病理学。结果显示TBI后GMF-KO小鼠的黑质酪氨酸羟化酶和多巴胺转运蛋白表达显着改善，并具有运动行为表现。另外，如核因子-kB的活化，诱导型一氧化氮合酶水平降低和环氧合酶-2表达所表明，神经炎症也明显减少。同样，与TBI后72小时相比，GMF-KO小鼠的神经营养素（包括脑源性神经营养因子和神经胶质源性神经营养因子）得到了显着改善。一致地，我们发现与TBI后72小时的GMF-KO小鼠相比，TBI增强了WT中的GFAP和UCHL-1表达，并减少了多巴胺能TH阳性神经元的数量。有趣的是，我们观察到WT的中位抬高的TH阳性单核细胞比GMF-KO小鼠减少。总体而言，我们发现缺少GMF可以显着逆转这些神经病理学事件并改善行为预后。这项研究提供的证据表明，PD诱导的病理学进展可在诱导TBI后开始。

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