Exo70 is a subunit of the greater exocyst complex, a collection of proteins that oversees cellular membrane addition and polarized exocytosis by acting as a tethering intermediate between the plasma membrane and newly synthesized secretory vesicles. Although Exo70 function has been implicated in several developmental events including cytokinesis and the establishment of cell polarity, its role in neuropathologies is poorly understood. On the other hand, traumatic brain injury is the result of mechanical external force including contusion, fast acceleration, and expansive waves that produce temporal or permanent cognitive damage and triggers physical and psychosocial alterations including headache, memory problems, attention deficits, difficulty thinking, mood swings, and frustration. Traumatic brain injury is a critical health problem on a global scale, constituting a major cause of deaths and disability among young adults. Trauma-related cellular damage includes redistribution of N-methyl-D-aspartate receptors outside of the synaptic compartment triggering detrimental effects to neurons. The exocyst has been related to glutamate receptor constitutive trafficking/delivery towards synapse as well. This work examines whether the exocyst complex subunit Exo70 participates in traumatic brain injury and if it is redistributed among subcellular compartments Our analysis shows that Exo70 expression is not altered upon injury induction. By using subcellular fractionation, we determined that Exo70 is redistributed from microsomes fraction into the synaptic compartment after brain trauma. In the synaptic compartment, we also show that the exocyst complex assembly and its interaction with GluN2B are increased. Finally, we show that the Exo70 pool that is redistributed comes from the plasma membrane. The present findings position Exo70 in the group of proteins that could modulate GluN2B synaptic availability in acute neuropathology like a traumatic brain injury. By acting as a nucleator factor, Exo70 is capable of redirecting the ensembled complex into the synapse. We suggest that this redistribution is part of a compensatory mechanism by which Exo70 is able to maintain GluN2B partially on synapses. Hence, reducing the detrimental effects associated with TBI pathophysiology.

中文翻译：

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反复轻度脑外伤后Exo70细胞内的重新分布

Exo70是更大的囊泡复合体的亚基，蛋白复合体通过充当质膜与新合成的分泌囊泡之间的束缚中间物，监督细胞膜的添加和极化的胞吐作用。尽管Exo70功能已牵涉到包括细胞分裂和细胞极性建立在内的若干发育事件中，但人们对其功能在神经病理学中的作用了解甚少。另一方面，颅脑外伤是机械外力的结果，包括挫伤，快速加速和扩张波，这些外力会产生暂时或永久的认知损伤，并引发身体和心理方面的改变，包括头痛，记忆力问题，注意力缺陷，思维困难，情绪摇摆和沮丧。在全球范围内，颅脑外伤是一个至关重要的健康问题，是年轻人死亡和致残的主要原因。创伤相关的细胞损伤包括N-甲基-D-天冬氨酸受体在突触区室外的重新分布，从而触发对神经元的有害作用。外囊也与谷氨酸受体组成性向突触的运输/递送有关。这项工作研究了囊外复合物亚基Exo70是否参与了颅脑外伤，并且是否在亚细胞区室中重新分布。我们的分析表明，损伤诱导后Exo70的表达没有改变。通过使用亚细胞分级分离，我们确定Exo70是从微粒体部分脑损伤后重新分配到突触室。在突触室 我们还表明，囊外复合体装配及其与GluN2B的相互作用增加了。最后，我们证明了重新分布的Exo70池来自质膜。目前的发现将Exo70定位在可以调节GluN2B突触在急性神经病理学（如脑外伤）中的蛋白质组中。通过充当成核因子，Exo70能够将整合的复合体重定向到突触中。我们建议这种重新分配是补偿机制的一部分，通过该机制Exo70能够在突触上部分维持GluN2B。因此，减少了与TBI病理生理学有关的有害作用。目前的发现将Exo70定位在可以调节GluN2B突触在急性神经病理学（如脑外伤）中的蛋白质组中。通过充当成核因子，Exo70能够将整合的复合体重定向到突触中。我们建议这种重新分布是补偿机制的一部分，通过该机制，Exo70能够在突触上部分维持GluN2B。因此，减少了与TBI病理生理学有关的有害作用。目前的发现将Exo70定位在可以调节GluN2B突触在急性神经病理学（如脑外伤）中的蛋白质组中。通过充当成核因子，Exo70能够将整合的复合体重定向到突触中。我们建议这种重新分配是补偿机制的一部分，通过该机制Exo70能够在突触上部分维持GluN2B。因此，减少了与TBI病理生理学有关的有害作用。我们建议这种重新分配是补偿机制的一部分，通过该机制Exo70能够在突触上部分维持GluN2B。因此，减少了与TBI病理生理学有关的有害作用。我们建议这种重新分布是补偿机制的一部分，通过该机制，Exo70能够在突触上部分维持GluN2B。因此，减少了与TBI病理生理学有关的有害作用。