Department of Neurosurgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China; Department of Neurosurgery, Jinling Hospital, School of medicine, Southern Medical University (Guangzhou), Nanjing, China.
Department of Neurosurgery, Changzheng Hospital, Second Military Medical University, Shanghai, China.
J Surg Res. 2020 Jan;245:321-329. doi: 10.1016/j.jss.2019.07.082. Epub 2019 Aug 14.
In the adult rodents' brain, CD24 expression is restricted to immature neurons located in the neurogenesis areas. Our previous studies have confirmed that CD24 expression could be markedly elevated in the cerebral cortex after traumatic brain injury (TBI) both in humans and in mice. Although there is a close relationship between CD24 and neurogenesis, it remains unknown about the specific role of CD24 in neurogenesis areas after TBI. Here, the expression of CD24 was detected in the ipsilateral hippocampus by the Western blotting and real-time quantitative polymerase chain reaction. RNA interference was applied to investigate the effects of CD24 on post-traumatic neurogenesis. Brain sections were labeled with CD24 and doublecortin (DCX) via immunofluorescence. The Morris water maze test was used to assess cognitive functions. The results indicated that both mRNA and protein levels of CD24 were markedly elevated in the hippocampus after TBI. Meanwhile, TBI could cause a decrease of DCX-positive cells in the dentate gyrus of the hippocampus. Downregulation of CD24 significantly inhibited the phosphorylation of Src homology region 2-containing protein tyrosine phosphatase 2 in the ipsilateral hippocampus. Meanwhile, inhibition of CD24 could reduce the number of DCX-positive cells in the dentate gyrus area and impair cognitive functions of the TBI mice. These data suggested that hippocampal expression of CD24 might positively regulate neurogenesis and improve cognitive functions after TBI.
在成年啮齿动物的大脑中，CD24 的表达仅限于神经发生区域中的未成熟神经元。我们之前的研究已经证实，在人类和小鼠的创伤性脑损伤（TBI）后，大脑皮层中的 CD24 表达可以明显升高。尽管 CD24 与神经发生密切相关，但 TBI 后 CD24 在神经发生区域中的具体作用仍不清楚。在这里，通过 Western blot 和实时定量聚合酶链反应检测对侧海马中 CD24 的表达。应用 RNA 干扰来研究 CD24 对创伤后神经发生的影响。通过免疫荧光将脑切片用 CD24 和双皮质素（DCX）标记。通过 Morris 水迷宫测试评估认知功能。结果表明，TBI 后海马中 CD24 的 mRNA 和蛋白水平均明显升高。同时，TBI 可导致海马齿状回中 DCX 阳性细胞减少。下调 CD24 可显著抑制同侧海马中 Src 同源结构域 2 含蛋白酪氨酸磷酸酶 2 的磷酸化。同时，抑制 CD24 可减少齿状回区 DCX 阳性细胞的数量，并损害 TBI 小鼠的认知功能。这些数据表明，海马中 CD24 的表达可能正向调节神经发生并改善 TBI 后的认知功能。
