Abstract 115
Background: Fas/CD95/Apo-1 is a cell surface receptor that transduces apoptotic death signals when cross-linked by its natural ligand. Fas-induced apoptosis has been implicated in the peripheral deletion of self reactive immune cells during development and in triggering apoptosis in immune privileged tissues. Apoptosis is also a major mechanism of neuronal loss following hypoxic-ischaemic injury (HII) to the developing brain. However, the role of Fas in neuronal apoptosis has not been studied in detail. Subject: We have investigated the expression of Fas in neuronal cells in vitro and in vivo using immunohistochemical methods and western blotting. Results: Fas was found to be expressed in neuronal PC12 cells in culture and in the 14 day old rat brain, with strongest expression in the cortex, hippocampus and cerebellum. Cross linking of Fas using agonist antibodies induced neuronal apoptosis both in vitro and in vivo. Finally, transient cerebral hypoxia-ischaemia resulted in a strong lateralized upregulation of Fas in the hippocampus, that peaked six hours after the insult. Conclusion: These results suggest that neuronal Fas was functional as a death receptor and may be involved in triggering neuronal apoptosis following HII to the developing brain.
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Felderhoff-Mueser, U., Greenwood, K., Taylor, D. et al. Increased Expression of Fas/CD95/APO-1 Following Hypoxic-Ischaemic Injury to the Developing Rat Brain. Pediatr Res 45, 906 (1999). https://doi.org/10.1203/00006450-199906000-00133
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DOI: https://doi.org/10.1203/00006450-199906000-00133