摘要
Background In response to the injury of the central nervous system （CNS）, the astrocytes upregulate the expression of glial fibrillary acidic protein （GFAP）, which largely contributes to the reactive gliosis after brain injury. The regulatory mechanism of this process is still not clear. In this study, we aimed to compare the ephrin-B2 deficient mice with the wild type ones with regard to qliosis after traumatic brain injury
Background In response to the injury of the central nervous system （CNS）, the astrocytes upregulate the expression of glial fibrillary acidic protein （GFAP）, which largely contributes to the reactive gliosis after brain injury. The regulatory mechanism of this process is still not clear. In this study, we aimed to compare the ephrin-B2 deficient mice with the wild type ones with regard to qliosis after traumatic brain injury
