Moon Younghye, Kim Joo Yeon, Choi So Yoen, Kim Kyungjin, Kim Hyun, Sun Woong
Department of Anatomy and Division of Brain Korea 21 Biomedical Science, Korea University College of Medicine, Seoul, Korea.
Neuroreport. 2011 Apr 20;22(6):304-8. doi: 10.1097/WNR.0b013e3283460265.
Traumatic brain injury promotes rapid induction of microglial cells and infiltration of peripheral macrophages to the injury sites. Such inflammatory responses are mediated by the activation and migration of immune cells, which are influenced by the actin cytoskeleton remodeling. In this study, we observed that the phosphorylation and expressions of ezrin-radixin-moesin (ERM) proteins, which are linkers for cell surface with actin cytoskeleton, are induced in the activated microglia/macrophages, whereas ERM molecules are only marginally expressed in quiescent microglia in the normal brain. These results suggest that ERM activation in the injury penumbra is implicated in the inflammatory immune responses after traumatic brain injury.
创伤性脑损伤会促使小胶质细胞迅速诱导生成，并使外周巨噬细胞浸润至损伤部位。此类炎症反应由免疫细胞的激活和迁移介导，而免疫细胞的激活和迁移受肌动蛋白细胞骨架重塑的影响。在本研究中，我们观察到埃兹蛋白-根蛋白-膜突蛋白（ERM），即细胞表面与肌动蛋白细胞骨架的连接蛋白，其磷酸化和表达在活化的小胶质细胞/巨噬细胞中被诱导，而ERM分子在正常大脑的静息小胶质细胞中仅微量表达。这些结果表明，损伤半暗带中的ERM激活与创伤性脑损伤后的炎症免疫反应有关。
