RESUMO
During the development of the brain, astrocytes acquire the ability to become reactive and form a scar. This change in the astrocytes occurs at approximately the same time that there is a decrease in the regenerative capacity of the CNS. Previous work from our laboratory had revealed that TAPA (Target of Anti-Proliferative Antibody, also known as CD81) is associated with reactive gliosis and the glial scar. TAPA is a member of the tetraspan family of proteins that appears to be associated with the regulation of cellular behavior. In order to define the role of TAPA in relation to the developmentally regulated CNS response to injury, we examined the levels of TAPA and GFAP immunoreactivity in rat pups that received a penetrating cerebral cortical injury. All of the animals injured at postnatal day 9 (PND 9), PND 18, or as adults, exhibited reactive gliosis scar formation when they were sacrificed 10 days after the cortical injury. Of the nine animals injured at PND 2, only three displayed reactive gliosis and scar formation. The remaining six rat pups had either a modest gliotic response or no detectable gliosis. The level of TAPA at the site of injury mimicked the reactive gliosis as defined by GFAP immunoreactivity. In all of the rats with a glial scar, there was a dramatic upregulation of TAPA that is spatially restricted to the reactive astrocytes. These results suggest that the upregulation of TAPA is an integral component of glial scar formation.
