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The Journal of Neuroscience, July 15, 2001, 21(14):4996-5006

FGF Induces a Switch in Death Receptor Pathways in Neuronal Cells

Eva M. Eves¹, Christine Skoczylas², Keiko Yoshida¹, Emad S. Alnemri³, and Marsha R. Rosner^{1, 2}

¹ Ben May Institute for Cancer Research and ² Department of Neurobiology, Pharmacology, and Physiology, University of Chicago, Chicago, Illinois 60637, and ³ Center for Apoptosis Research and Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107

Basic fibroblast growth factor (FGF2) has many roles in neuronal development and maintenance including effects on mitogenesis, survival, fate determination, differentiation, and migration. Using a conditionally immortalized rat hippocampal cell line, H19-7, and primary hippocampal cultures, we now demonstrate that FGF2 treatment differentially regulates members of the tumor necrosis factor (TNF) superfamily of death domain receptors and their ligands. H19-7 cells transferred from serum to defined (N2) medium undergo apoptosis by a Fas-dependent mechanism similar to primary neurons. In contrast, H19-7 cells treated with FGF undergo apoptosis by a Fas-independent mechanism. FGF suppresses the Fas death pathway but also induces apoptosis by activation of a TNF death pathway in both H19-7 and hippocampal progenitor cells. Expression of the TNF receptor 1 (TNFR1) or TNFR2 in H19-7 cells is sufficient to sensitize the cells to TNF, similar to the effects of FGF. Because TNF can be either proapoptotic or antiapoptotic, these results provide an explanation for the divergent trophic effects of FGF2 treatment and the observation that multiple trophic inputs are required for the survival of specific neurons.

Key words: TNF; TNFR1; Fas; FasL; FGF; neuronal cell line; H19-7; apoptosis; hippocampal cells

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21144996-11$05.00/0

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