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首页> 外文期刊>The European Journal of Neuroscience >Granulocyte macrophage colony-stimulating factor treatment results in recovery of motor function after white matter damage in mice
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Granulocyte macrophage colony-stimulating factor treatment results in recovery of motor function after white matter damage in mice

机译：粒细胞巨噬细胞集落刺激因子治疗可导致小鼠白质损伤后运动功能恢复

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摘要

Clinical stroke usually results from a cerebral ischaemic event, and is frequently a debilitating condition with limited treatment options. A significant proportion of clinical strokes result from specific damage to the subcortical white matter (SWM), but currently there are few animal models available to investigate the pathogenesis and potential therapeutic strategies to promote recovery. Granulocyte macrophage colony-stimulating factor (GM-CSF) is a cytokine that has been previously shown to promote neuroprotective effects after brain damage; however, the mechanisms mediating this effect are not known. Here, it is reported that GMCSF treatment results in dramatic functional improvement in a white matter model of stroke in mice. SWM stroke was induced in mice by unilateral injections of the vasoconstrictor, endothelin-1 (ET-1). The results reveal that ET-1-induced stroke impairs skilled motor function on the single pellet-reaching task and results in forelimb asymmetry, in adult mice. Treatment with GM-CSF, after stroke, restores motor function and abolishes forelimb asymmetry. The results also indicate that GM-CSF promotes its effects by activating mammalian target of rapamycin signalling mechanisms in the brain following stroke injury. Additionally, a significant increase in GM-CSF receptor expression was found in the ipsilateral hemisphere of the ET-1-injected brain. Taken together, the present study highlights the use of an under-utilized mouse model of stroke (using ET-1) and suggests that GM-CSF treatment can attenuate ET-1-induced functional deficits.
机译：临床中风通常是由脑缺血事件引起的，通常是使人衰弱的疾病，治疗选择有限。临床卒中的很大一部分是由皮层下白质（SWM）的特异性损伤引起的，但是目前很少有动物模型可用于研究发病机理和促进康复的潜在治疗策略。粒细胞巨噬细胞集落刺激因子（GM-CSF）是一种细胞因子，先前已被证明可以促进脑损伤后的神经保护作用。但是，尚不知道介导此作用的机制。在这里，据报道，GMCSF治疗在小鼠中风的白质模型中导致了显着的功能改善。通过单侧注射血管收缩剂内皮素-1（ET-1）在小鼠中诱发SWM中风。结果表明，在成年小鼠中，ET-1诱发的中风会损害单次药丸到达任务的熟练运动功能，并导致前肢不对称。中风后，GM-CSF治疗可恢复运动功能并消除前肢不对称性。结果还表明，GM-CSF通过激活中风损伤后大脑中雷帕霉素信号传导机制的哺乳动物靶标来促进其作用。另外，在注射了ET-1的大脑的同侧半球中发现了GM-CSF受体表达的显着增加。综上所述，本研究强调了未充分利用的中风小鼠模型（使用ET-1）的使用，并建议GM-CSF治疗可以减轻ET-1诱导的功能缺陷。

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