Abstract
It is considered that necrosis and degeneration of neurons resulting from traumatic brain injury induces secondary swelling of astrocytes, endothelial cell injury and brain edema from destruction of the BBB (blood brain barrier) . The process of inducing brain edema might be related to not only regressive changes of cells but also accelerated reparation of cells and tissues. To clarify the reparation mechanism of cells and tissues in the central nervous system after brain injury, we studied the expression of the ERM ( Ezurin /Radixin /Moesin ) family proteins which is one of the factors of signal transduction on the brain cold injury model. We used 21 rat cold injury models (control : 3, sham operation 3, Day 1: 3, Day 4 : 3, Day 7 : 3, Day 10 : 3, Day 14 : 3), and each specimen was examined immunohistochemically using anti-ERM antibodies. To identify the cell, double staining was performed using GFAP and NF (neurof filament) . Ezurin was expressed in the peripheral areas of the injured brain and hippocampus from day 4. Radaxin was expressed in the ipsilateral hippocampus from day 7. Moesin was expressed in the peripheral areas of the injured brain from day 4, although it was not expressed in the control specimens. In the study of double staining, the ERM ( Ezurin/Radixin/Moesin) proteins were detected in the GFAP positive cells but not in the NF positive cells. In addition, Moesin positive cells were stained with PCNA (proliferaing cell nuclear antigen) . It is suggested that the expression of ERM family proteins which lines cell attachment may play an important role in signal communication between neurons and astrocytes after brain injury.
