Fibronectin and Laminin Increase in the Mouse Brain after Controlled Cortical Impact Injury

The complex environment of the traumatically injured brain exhibits aspects of inhibition and ongoing cell death together with attempts at repair and regeneration. Elucidating these events and exploiting those factors involved in endogenous repair and regeneration may aid in developing more effective treatments for traumatic brain injury. Two extracellular matrix proteins critical to neural development—fibronectin and laminin—may also play a protective or reparative role in the injury response. While both of these proteins have been found to increase following human brain injury, the presence of these proteins has not been studied in a clinically-relevant animal model of blunthead trauma. In this study, we examined the spatiotemporal profile of both fibronectin and laminin in the mouse brain following controlled cortical impact injury. Fibronectin and laminin reactivity was localized to the injury penumbra up to 14 days post-injury and was significantly higher than uninjured controls at 3 days post-injury. Upon examining the spatial relationship of fibronectin and laminin to support cells, we found macrophages/activated microglia prominently present in the fibronectin-rich tissue, consistent with a role for fibronectin in facilitating debris clearing. Furthermore, reactive astrocyte processes were found sheathing laminin positive vasculature, suggesting that laminin may play a role in repairing the blood–brain barrier. These and other hypothesized reparative roles for fibronectin and laminin after traumatic brain injury are discussed.