Coordination of fibroblast growth factor receptor 1 (FGFR1) and fibroblast growth factor-2 (FGF-2) trafficking to nuclei of reactive astrocytes around cerebral lesions in adult rats.

Traumatic injury to the adult central nervous system initiates a cascade of cellular and trophic events, culminating in the formation of a reactive gliotic scar through which transected axons fail to regenerate. Levels of fibroblast growth factor-2 (FGF-2), a potent gliogenic and neurotrophic factor, together with its full-length receptor, FGF receptor 1 (FGFR1) are coordinately and significantly increased postinjury in both nuclear and cytoplasmic fractions of extracted cerebral cortex biopsies after a penetrant injury. FGFR1 is colocalized with FGF-2 in the nuclei of reactive astrocytes, and here FGF-2 is associated with nuclear euchromatin. This study unequivocally demonstrates coordinate up-regulation and trafficking of FGF-2 and full-length FGFR1 to the nucleus of reactive astrocytes in an in vivo model of brain injury, thereby implicating a role in nuclear activity for these molecules. However, the precise contribution of nuclear FGF-2/FGFR1 to the pathophysiological response of astrocytes after injury is undetermined.