Armcx1 is a member of the ARMadillo repeat-Containing protein on the X chromosome (ARMCX) family, which is recognized to have evolutionary conserved roles in regulating mitochondrial transport and dynamics. Previous research has shown that Armcx1 is expressed at higher levels in mice after axotomy and in adult retinal ganglion cells after crush injury, and this protein increases neuronal survival and axonal regeneration. However, its role in traumatic brain injury (TBI) is unclear. Therefore, the aim of this study was to assess the expression of Armcx1 after TBI and to explore possible related mechanisms by which Armcx1 is involved in TBI. We used C57BL/6 male mice to model TBI and evaluated the role of Armcx1 in TBI by transfecting mice with Armcx1 small interfering RNA (siRNA) to inhibit Armcx1 expression 24 h before TBI modeling. Western blotting, immunofluorescence, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, Nissl staining, transmission electron microscopy, adenosine triphosphate (ATP) level measurement, neuronal apoptosis analysis, neurological function scoring and the Morris water maze were performed. The results demonstrated that Armcx1 protein expression was elevated after TBI and that the Armcx1 protein was localized in neurons and astroglial cells in cortical tissue surrounding the injury site. In addition, inhibition of Armcx1 expression further led to impaired mitochondrial transport, abnormal morphology, reduced ATP levels, aggravation of neuronal apoptosis and neurological dysfunction, and decrease Miro1 expression. In conclusion, our findings indicate that Armcx1 may exert neuroprotective effects by ameliorating neurological injury after TBI through a mitochondrial transport pathway involving Miro1.

中文翻译：

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Armcx1 通过涉及 Miro1 的线粒体运输途径减少脑外伤后的神经损伤

Armcx1 是 X 染色体上 ARMadillo 重复序列蛋白 (ARMCX) 家族的成员，该家族被认为在调节线粒体运输和动力学方面具有进化保守的作用。先前的研究表明，Armcx1 在轴索切除后的小鼠和挤压损伤后的成人视网膜神经节细胞中表达水平较高，并且这种蛋白质可增加神经元存活和轴突再生。然而，其在创伤性脑损伤（TBI）中的作用尚不清楚。因此，本研究的目的是评估TBI后Armcx1的表达，并探讨Armcx1参与TBI的可能相关机制。我们使用C57BL/6雄性小鼠进行TBI建模，并通过在TBI建模前24小时用Armcx1小干扰RNA（siRNA）转染小鼠以抑制Armcx1表达来评估Armcx1在TBI中的作用。进行蛋白质印迹、免疫荧光、末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色、尼氏染色、透射电镜、三磷酸腺苷（ATP）水平测量、神经元凋亡分析、神经功能评分和Morris水迷宫。结果表明，TBI 后 Armcx1 蛋白表达升高，并且 Armcx1 蛋白定位于损伤部位周围皮质组织的神经元和星形胶质细胞中。此外，抑制Armcx1表达进一步导致线粒体运输受损、形态异常、ATP水平降低、神经元凋亡和神经功能障碍加剧，以及Miro1表达降低。总之，我们的研究结果表明，Armcx1 可能通过涉及 Miro1 的线粒体转运途径改善 TBI 后的神经损伤，从而发挥神经保护作用。