title: Gliosis after traumatic brain injury in conditional ephrinB2-knockout mice.
abstract: 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 gliosis after traumatic brain injury.
  
  
  METHODS
  We generated ephrin-B2 knockout mice specifically in CNS astrocytes. Twelve mice from this gene-knockout strain were randomly selected along with twelve mice from the wild type littermates. In both groups, a modified controlled cortical impact injury model was applied to create a closed traumatic brain injury. Twenty-eight days after the injury, Nissl staining and GFAP immunofluorescence staining were used to compare the brain atrophy and GFAP immunoreactivity between the two groups. All the data were analyzed by t-test for between-group comparison.
  
  
  RESULTS
  We successfully set up the conditional ephrin-B2 knockout mice strain, which was confirmed by genotyping and ephrin-B2/GFAP double staining. These mice developed normally without apparent abnormality in general appearance. Twenty-eight days following brain injury, histopathology revealed by immunohistochemistry showed different degrees of cerebral injuries in both groups. Compared with wild-type group, the ephrin-B2 knockout group exhibited less brain atrophy ratio for the injured hemispheres (P = 0.005) and hippocampus (P = 0.027). Also the wild-type group demonstrated greater GFAP immunoreactivity increment within hippocampal regions (P = 0.008).
  
  
  CONCLUSIONS
  The establishment of conditional ephrin-B2 knockout mice provides us with a new way to explore the role of ephrin-B2 in astrocytes. Our findings revealed less atrophy and GFAP immunoreactivity in the knockout mice strain after traumatic brain injury, which implied ephrin-B2 could be one of the promoters to upregulate gliosis following brain injury.
authors.affiliation: Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Liu
authors.forename: Xiao-Lin
authors.initials: XL
authors.lastname: Chen
authors.forename: Jian-Kai
authors.initials: JK
authors.lastname: Yang
authors.forename: Ze-Guang
authors.initials: ZG
authors.lastname: Ren
authors.forename: Shuo
authors.initials: S
authors.lastname: Wang
mesh_terms: D000818:Animals; D001284:Atrophy; D001921:Brain / Q000473:pathology; D001930:Brain Injuries / Q000150:complications* / Q000473:pathology; D036388:Ephrin-B2 / Q000172:deficiency / Q000502:physiology*; D005904:Glial Fibrillary Acidic Protein; D005911:Gliosis / Q000209:etiology*; D007150:Immunohistochemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000032:analysis
chemical_list: D036388:Ephrin-B2; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; C528900:glial fibrillary astrocytic protein, mouse