Martinez G, Di Giacomo C, Sorrenti V, Carnazza M L, Ragusa N, Barcellona M L, Vanella A
Department of Anatomy, Diagnostic Pathology, Legal Medicine, Public Health (G. Ingrassia 1510-1580 Anatomist), Catania, Italy.
J Neurosci Res. 2001 Jan 15;63(2):136-42. doi: 10.1002/1097-4547(20010115)63:2<136::AID-JNR1005>3.0.CO;2-4.
Several trophic factors are known to regulate the survival and growth of neurons in brain and peripheral tissues. Several findings suggest that basic fibroblast growth factor-2 (FGF-2) plays an important role in the "self-repair" responses that follow injuries such as trauma and brain ischemia and that FGF-2 contributes to the repair of damaged tissue. Transforming growth factor-beta (TGF-beta) is a potent growth-regulatory protein secreted by virtually all cells. In the present study, we used immunohistochemical techniques to investigate whether FGF-2 and TGF-beta1 participate in the healing of damaged tissue following partial brain ischemia. The profile of the observed immunoreactivities indicated that TGF-beta1 and FGF-2 release varies between the different cerebral areas subjected to ischemic insult. Moreover, the sectorial heterogeneity of immunocytochemical response suggests that, during postischemic reperfusion, neuronal recovery may be due not only to neuron-glia interaction but also to neurochemical conditions involving inhibitory interneurons.